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Cold exposure: Human immune responses and intracellular cytokine expression
Abstract
It is commonly believed that exposure to cold environmental temperatures depresses immune function and increases the risk for infection. This review paper will 1) present an overview of human physiological responses to cold exposure, 2) present the human studies examining the effects of cold exposure on immune responses, and 3) summarize recent experiments from our laboratories examining the effects of exercise and fatigue on immune responses during subsequent cold exposure. Based on the review of the literature, there is no support for the concept that cold exposure depresses immune function.
... There was a trend of increased neutrophil count in HHct ewes only at 7 d (P > 0.05) after transport to moderate altitude (Fig. 2) which is consistent with the reported increase in neutrophil numbers in response to cold air exposure (Castellani et al., 2002). The slight rise in circulating neutrophils following moderate altitude exposure in HHct ewes may be attributed to cortisol mediated demargination of neutrophils. ...
... The tendency of increased N/L ratio at 7d in HHct ewes after transport is consistent with the tendency of increased cortisol levels at that time, and represent a leukocyte response to moderate altitude exposure (Fig. 4). Also, cold exposure has been reported to increase norepinephrine concentration (Castellani et al., 2002). Therefore, it seems that both norepinephrine and cortisol mediate the observed trend of increase in N/L ratio on d 7 after altitude exposure. ...
... Monocyte numbers, similar to lymphocyte numbers, showed a trend towards decline at 7 d after transport in MHct ewes only compared to baseline levels (Fig. 5). Castellani et al. (2002) reported variable changes in monocyte counts and concluded that norepinephrine accounted for most of the variance in leukocyte subsets during cold exposure. The observed decline in MHct ewes at 7 d after transport to moderate altitude may indicate higher rate of transmigration from circulation to other tissues and better immune surveillance compared to the other groups. ...
Moneva, P., Yanchev, I. & Metodiev, N. (2023). Dynamics of leukocytes and cytokines after moderate altitude exposure in pregnant ewes with low and high hematocrit levels. Bulg. J. Agric. Sci., 29(4), 723-732 The object of the present study was to investigate leukocyte subsets distribution and the dynamics of some pro-inflamma-tory and anti-inflammatory cytokines in response to moderate altitude exposure in sheep having different hematocrit values. Thirty Ile De France ewes were selected from an experimental herd according to their hematocrit levels and were allocated into 3 groups as follows: low hematocrit (LHct) group (hematocrit range 19.7-27.9 %), high hematocrit (HHct) group (hematocrit range 32.0-36.9 %) and mean hematocrit (MHct) group (hematocrit range 28.3-29.8 %). Immediately after shearing, ewes were transported from the Institute farm (altitude 500 m) to a mountain pasture (altitude 1440 m). Blood samples were taken by jugular venepuncture at the following time points: before transportation (baseline level), on day 7, 20 and 42 after the transport. The traits investigated were leukocyte subsets (basophils, eosinophils, neutrophils, lymphocytes, monocytes, large immature cells) and cytokines (IL-2, Il-4, IL-6, IL-10, IL-17A, IFN-γ, TNF-α). Moderate altitude exposure elicited significant decrease in lymphocyte numbers in all the 3 groups at d 7 after transport to moderate altitude followed by a return to normal levels at d 20 after transport. Neutrophil numbers were not influenced by moderate altitude hypoxia. There was hematocrit associated changes in basophil, eosinophil and monocyte numbers suggesting different trafficking patterns of these leukocyte subsets. There was a tendency of slight increase in large immature cells in HHct ewes at d 7. There was a relation between N/L ratio and large immature cells as follow: baseline levels (r = 0.627995, P < 0.01); at 7 d (r = 0.771221, P < 0.001); at 20 d (r = 0.606801, P < 0.01); at 42 d (r = 0.566646, P < 0.01). IL-10 levels in HHct and MHct ewes tended to decrease at 7 d compared to basal levels. There was relation between IL-2 and IL-6 at 20 d (r = 0.531371, P < 0.01) and 42 d (r = 0.586212, P < 0.01). Investigated pro-inflammatory Th17 (IL-17A) and Th1 cytokines (IL-2, IL-6, IFN-γ, TNF-α), as well as anti-inflammatory Th2 cytokines (IL-4 and IL-10) were not influenced by moderate altitude exposure. The results are interpreted to suggest that exposure of pregnant ewes at ambient temperature below the lower critical temperature at moderate altitude prevents cytokines increase.
... Hypothermic stress as a result of exposure to cold environments and cold water has been shown to increase circulating catecholamine concentration and subsequently influence lymphocyte mobilisation (Jansky et al. 1996;Castellani et al. 2002). Our results found that PBC stimulated a greater change in numbers of CD16 + NK cells and CD8 + T cells in comparison to CWI, suggesting a larger catecholamine response after PBC could result in a morepronounced mobilisation of lymphocytes than CWI. ...
... Our results found that PBC stimulated a greater change in numbers of CD16 + NK cells and CD8 + T cells in comparison to CWI, suggesting a larger catecholamine response after PBC could result in a morepronounced mobilisation of lymphocytes than CWI. This response is similar to that found after exposure to other stressful stimuli, such as exercise, injury, or psychological stressors (Castellani et al. 2002;Dhabhar 2002;Dhabhar et al. 2012). CD16 + NK cells in this study were observed to increase by 167% after PBC, 58% after CWI, and 29% after CON. ...
Partial body cryotherapy (PBC) is proposed to alleviate symptoms of exercise-induced muscle damage (EIMD) by reducing associated inflammation. No studies have assessed acute PBC exposure on peripheral blood mononuclear cell mobilisation or compared these with cold water immersion (CWI), which may inform how PBC impacts inflammatory processes. This trial examined the impact of a single PBC exposure on circulating peripheral blood mononuclear cells compared to CWI or a control. 26 males were randomised into either PBC (3 min at − 110 to − 140 °C), CWI (3 min at 9 °C), or control (3 min at 24 °C), with blood samples, heart rate, and blood pressure taken before and after exposure. Cytometric analysis determined that CD8⁺ T-cell populations were significantly elevated after treatments, with PBC increasing CD8⁺ T cells to a greater degree than either CWI or CON. Natural killer cell counts were also elevated after PBC, with the increase attributed specifically to the CD56loCD16⁺ cytotoxic subset. This provides the first evidence for the effect of PBC exposure on redistribution of immune cells. An increase in circulating leukocyte subsets such as CD8⁺ T cells and CD56loCD16⁺ natural killer cells suggests that PBC may induce a transient mobilisation of lymphocytes. PBC may thus enable a more efficient trafficking of these cells from the circulation to the site of initial cellular insult from exercise, potentially accelerating the process of cellular recovery. This provides novel evidence on the use of PBC as a recovery treatment and may also have applicability in other clinical settings involving the recovery of damaged skeletal muscle.
... [12] However, the findings concerning the effects of cold exposure on human immune function are inconsistent. [13] The exposure of macrophages (in vitro) to a temperature of 24°C for 1 hour led to a decrease in phagocytic activity; moreover, the exposure of peritoneal macrophages (in vitro) to temperatures of 4, 10, 24, and 37°C for 1 hour suggested a close inverse association between incubation temperature and the number of cells capable of phagocytosis. [14] Polderman [15] stated that a decline in core body temperature causes leukocytopenia, suppressed phagocytosis, and reduced release of cytokines-factors that increase host susceptibility to infection. ...
Climate and temperature have long been considered in relation to human diseases and mortality. In this study, we investigated whether daily temperature and humidity and patients’ personal history affect the volume of peritonsillar abscesses (PTAs). We included 52 patients with PTAs who were admitted to the emergency department of the study hospital; their computed tomography data were analyzed, and PTA volume was measured. We investigated the possible correlation between PTA volume and mean/minimum/maximum temperature and humidity. Furthermore, we obtained personal history data, including information on drinking status, smoking status, dental problems, and patients’ treatment experiences at local clinics before visiting the emergency department. The mean PTA volume was 3.93 mL, which was significantly correlated with temperature differences between 1 and 2 days before hospitalization and the day of hospitalization (P < .05) and also with a lack of treatment experience at local clinics (P < .001). However, no significant correlation was noted between PTA volume and the mean/minimum/maximum temperature and humidity on the day of hospitalization (P > .05). Similar findings were obtained for drinking status, smoking status, and dental problems (P > .1). PTA volume appears to be strongly associated with temperature differences between 1 and 2 days before hospitalization and the day of hospitalization. Patients with treatment experience at local clinics exhibited substantial increases in PTA volume. Thus, an increased PTA volume may be observed in patients who visit the emergency department without any treatment experience at local clinics or from environments that differ considerably from their current environment in terms of temperature.
... The authors suggest that longer immersions impose compound stress on the body, highlighting possible immunostimulatory effects of the cold. 63 Considering that IL-6 is released from inflammatory cells and the endothelium during an injury or infection, it is assumed that it exerts a proinflammatory function, in addition of being related to delayed-onset muscle soreness. 64 It is thought that the reduction in muscle blood flow caused by CWI prevents the clearance of IL-6 produced by the muscle. ...
Objective:
Our objective was to determine the efficacy of cold-water immersion (CWI) on the management of muscle soreness to identify the impact of immersion time, water temperature, CWI protocol, and type of exercise on this outcome.
Design:
Intervention systematic review and meta-analysis.
Setting:
MEDLINE/PubMed, Embase, Central, and SPORTDiscus databases were searched from their earliest record to July 30, 2020. Only randomized controlled trials that assessed muscle soreness comparing CWI and control were included. Studies were pooled in different subgroups regarding the used protocol: water temperature (severe or moderate cold), immersion time (short, medium, or longer time), CWI protocol (intermittent or continuous application), and type of exercise (endurance or resistance exercise). Data were pooled in a meta-analysis and described as weighted mean difference (95% confidence interval, P < 0.05).
Participants:
Athletes and nonathletes.
Interventions:
Cold-water immersion and control condition.
Main outcome measures:
Muscle soreness.
Results:
Forty-four studies were included. For immediate effects, CWI was superior to control regardless of water temperature and protocol, and for short and medium immersion times and endurance exercises. For delayed effects, CWI was superior to control in all subgroups except longer immersions time.
Conclusions:
This study suggests that CWI is better than control for the management of muscle soreness and water temperature and CWI protocol do not influence this result, but only short and medium immersions times presented positive effects. Aiming immediate effects, the best results suggest CWI application only after endurance exercises, while delayed effect CWI was superior both after endurance and resistance exercises.
... Evidence suggests both a suppressive and supportive effect of cold environmental temperature on the immune system, which partly depends on the length of the cold exposure. Several studies suggested that while short-term cold stimulation decreases human lymphoproliferative response and Th1 cytokine production [49,50], it also provokes inflammatory responses and immunosuppressive signature genes [51,52]. In line with the data from mice, long-term adaptation to cold exposure induces an anti-inflammatory reaction [14], implying that the shift in the immune response during cold adaptation may be of general importance. ...
Cancer immunotherapies emerge as promising strategies for restricting tumour growth. The tumour microenvironment (TME) has a major impact on the anti‐tumour immune response and on the efficacy of the immunotherapies. Recent studies have linked changes in the ambient temperature with particular immuno‐metabolic reprogramming and anti‐cancer immune response in laboratory animals. Here, we describe the energetic balance of the organism during change in temperature, and link this to the immune alterations that could be of relevance for cancer, as well as for other human diseases. We highlight the contribution of the gut microbiota in modifying this interaction. We describe the overall metabolic response and underlying mechanisms of tumourigenesis in mouse models at varying ambient temperatures and shed light on their potential importance in developing therapeutics against cancer.
... All the GO terms were related to migrations of white blood cell subtypes such as leukocyte migration (Table 3); thus, molecules involved in immune functions may be activated by the cold exposure experiments. In fact, it has been reported that acute mild cold stress may affect the proliferation of several white blood cell subtypes although effects of the proliferation on host defense remain unknown [49]. Incidentally, the expression change in the CD177 molecule (CD177) gene was the most statistically significant (FDR = 6.46×10 -5 ) in the differential expression analysis. ...
Background:
Physiological thermoregulatory systems in humans have been a key factor for adaptation to local environments after their exodus from Africa, particularly, to cold environments outside Africa. Recent studies using high-throughput sequencing have identified various genes responsible for cold adaptation. However, the molecular mechanisms underlying initial thermoregulation in response to acute cold exposure remain unclear. Therefore, we investigated transcriptional profiles of six young Japanese male adults exposed to acute cold stress.
Methods:
In a climatic chamber, the air temperature was maintained at 28°C for 65 min and was then gradually decreased to 19°C for 70 min. Saliva samples were obtained from the subjects at 28°C before and after 19°C cold exposure and were used for RNA sequencing.
Results:
In the cold exposure experiment, expression levels of 14 genes were significantly changed [false discovery rate (FDR) < 0.05] although the degree of transcriptional changes was not high due to experimental conditions or blunted transcriptional reaction in saliva to cold stress. As a result, differential gene expression analyses detected the cathepsin L (CTSL) gene to be significantly upregulated, with FDR < 0.05 and log2 fold change value > 1; thus, this gene was identified as a differentially expressed gene. Given that the cathepsin L protein is related to invasion of the novel coronavirus (SARS-CoV-2), mild cold stress might alter the susceptibility to coronavirus disease-19 in humans. The gene ontology enrichment analysis for 14 genes with FDR < 0.05 suggested that immune-related molecules could be activated by mild cold stress.
Conclusions:
The results obtained from this study indicate that CTSL expression levels can be altered by acute mild cold stress.
... While repeated exercise in a cold climate has been shown to cause local signs of airway inflammation [27--27-29], the systemic immune effects are more uncertain [30]. Generally, short-duration, moderate-intensity exercise at room temperature has not been shown to negatively affect systemic immune function [31,32]. ...
Exposure to a cold climate is associated with an increased morbidity and mortality, but the specific mechanisms are largely unknown. People with cardiopulmonary disease and winter endurance athletes are particularly vulnerable. This study aimed to map multiple domains of airway responses to exercise in subzero temperature in healthy individuals.
Thirty-one healthy subjects underwent whole-body exposures for 50 minutes on two occasions in an environmental chamber with intermittent moderate-intensity exercise in +10 °C and -10 °C. Lung function, plasma/urine CC16 , and symptoms were investigated before and after exposures.
Compared to baseline, exercise in -10 °C decreased FEV1 (p=0.002), FEV1/FVC (p<0.001), and increased R20Hz (p=0.016), with no differences between exposures. Reactance increased after +10 °C (p=0.005), which differed (p=0.042) from a blunted response after exercise in -10 °C. Plasma CC16 increased significantly within exposures, without differences between exposures. Exercise in -10 °C elicited more intense symptoms from the upper airways, compared to +10 °C. Symptoms from the lower airways were few and mild.
Short-duration moderate-intensity exercise in -10 °C induces mild symptoms from the lower airways, no lung function decrements or enhanced leakage of biomarkers of airway epithelial injury, and no peripheral bronchodilatation, compared to exercise in +10 °C.
Objectives:
Evaluating whether meteorological and geographical variables could be associated with the severity of COVID-19 in Spain.
Methods:
An ecological study was performed to analyze the influence of meteorological and geographical factors in hospital admissions and deaths due to COVID-19 in the 52 provinces of Spain (24 coastal and 28 inland regions), during the first three pandemic waves. Medical and mortality data were collected from the Carlos III Health Institute (ISCIII) and meteorological variables were requested to the Spanish State Meteorological Agency (AEMET).
Results:
Regarding the diagnosed cases it is remarkable that the percentage of patients hospitalized for COVID-19 was lower in the coastal provinces than in the inland ones (8.7 ± 2.6% vs. 11.5 ± 2.6%; p = 9.9 × 10-5). Furthermore, coastal regions registered a lower percentage of mortality than inland regions (2.0 ± 0.6% vs. 3.1 ± 0.8%; p = 1.7 × 10-5). Mean air temperature was inversely correlated both with COVID-19 hospitalizations (Rho: -0.59; p = 3.0 × 10-6) and mortality (Rho: -0.70; p = 5.3 × 10-9). In those provinces with a mean air temperature <10 °C mortality by COVID-19 was twice that of those with >16 °C. Finally, we found an association between mortality and the location of the province (coastal/inland), altitude, patient age and the average air temperature; the latter was inversely and independently correlated with mortality (non standardised B coeff.: -0.24; IC 95%: -0.31 to -0.16; p = 2.38 × 10-8).
Conclusions:
The average air temperature was inversely associated with COVID-19 mortality in our country during the first three waves of the pandemic.
Resumen
Objetivos: Evaluar si factores meteorológicos y geográficos pudieron relacionarse con la gravedad de la COVID-19 en España.
Métodos: Estudio ecológico, a escala provincial, que analiza la influencia de factores meteorológicos y geográficos en la hospitalización y mortalidad por COVID-19 en las 52 provincias españolas (24 costeras y 28 del interior), durante las tres primeras olas. Los datos de hospitalizaciones y mortalidad se obtuvieron del Instituto de Salud Carlos III (ISCIII). Los datos epidemiológicos del Instituto Nacional Estadística (INE) y la Red Nacional de Vigilancia Epidemiológica (RENAVE). Las variables meteorológicas de la Agencia estatal de meteorología (AEMET).
Resultados: El porcentaje de pacientes hospitalizados por COVID-19, del total de personas infectadas, fue inferior en las provincias costeras que en las del interior peninsular (8,7±2,6% vs. 11,5 ±2,6%; p=9,9x10⁻⁵). De igual manera la costa registró menor porcentaje de mortalidad que el interior peninsular (2,0±0,6% vs. 3,1±0,8%; p=1,7x10⁻⁵). La temperatura media correlacionó negativamente con la hospitalización (Rho: -0,59; p=3,0x10⁻⁶) y la mortalidad por COVID-19 (Rho: -0,70; p=5,3x10⁻⁹). Las provincias con una temperatura media <10ºC duplicaron la mortalidad por COVID respecto a las de >16ºC. La mortalidad se relacionó con la localización provincial (costa/interior), la altitud, la edad de la población y la temperatura media, siendo esta última la variable asociada de manera independiente (Coef. B no estandarizado: -0,24; IC 95%: -0,31 a -0,16; p=2,38x10⁻⁸).
Conclusiones: La mortalidad por COVID-19 durante las tres primeras olas de la pandemia en nuestro país se asoció inversamente con la temperatura media.
White adipocytes store energy differently than brown and brite adipocytes which dissipate energy under the form of heat. Studies have shown that adipocytes are able to respond to bacteria thanks to the presence of Toll-like receptors at their surface. Despite this, little is known about the involvement of each class of adipocytes in the infectious response. We treated mice for one week with a β3-adrenergic receptor agonist to induce activation of brown adipose tissue and brite adipocytes within white adipose tissue. Mice were then injected intraperitoneally with E. coli to generate acute infection. The metabolic, infectious and inflammatory parameters of the mice were analysed during 48 hours after infection. Our results shown that in response to bacteria, thermogenic activity promoted a discrete and local anti-inflammatory environment in white adipose tissue characterized by the increase of the IL-1RA secretion. More generally, activation of brown and brite adipocytes did not modify the host response to infection including no additive effect with fever and an equivalent bacteria clearance and inflammatory response. In conclusion, these results suggest an IL-1RA-mediated immunomodulatory activity of thermogenic adipocytes in response to acute bacterial infection and open a way to characterize their effect along more chronic infection as septicaemia.
The effects of β-adrenoceptor agonists (β-agonists) on the production of tumor necrosis factor-α (TNF-α), interleukin-1 β (IL-1β) and interleukin-8 (IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMCs) were investigated. The β-agonists, procaterol, clenbuterol, fenoterol and terbutaline, inhibited TNF-α and IL-1β production in a concentration-dependent manner, whereas they had no effect on IL-8 production. TNF-α production was inhibited more potently than IL-1β. Dibutyryl cyclic AMP (dbcAMP) also inhibited the production of TNF-α and IL-1β, but not IL-8. TNF-α production was almost completely inhibited by dbcAMP, whereas IL-1β production appeared to be partially refractory even at the highest concentration examined. Both procaterol and the-ophylline elevated cAMP levels in LPS-stimulated PBMCs, but the effect of procaterol was limited. The inhibition of TNF-α and IL-1β production by procaterol was additively potentiated with theophylline. dl-Propranolol, a β-adrenoceptor antagonist, abrogated the inhibition of TNF-α and IL-1β production by procaterol. These results indicate that β-agonists inhibit the production of proinflammatory cytokines, such as TNF-α and IL-1β, by elevating intracellular cAMP levels. These properties of β-agonists might be beneficial in the treatment of allergic inflammation.
Abstract Endotoxin activates white blood cells and complement and produces a spectrum of clinical syndromes ranging from fever to septic shock. Although production of endogenous endotoxemia during cardiopulmonary bypass (CPB) has recently been reported, the role of hypothermia on endotoxemia is not clear. In this study, we evaluated the effects of moderate (24–28°C) and mild (32–34°C) hypothermia on blood endotoxin levels. The study population consisted of 20 patients who underwent coronary artery bypass grafting (CABG) with CPB. Moderate systemic hypothermia was applied during aortic cross-clamping in ten patients (group 1) and mild hypothermia in the remaining ten patients (group 2). The mean rectal temperatures were 26.8 ± 1.2°C in group 1 and 33.8 ± 0.8°C in group 2. The blood samples for endotoxin level measurements were obtained before CPB, during aortic cross-clamping, immediately after the release of the cross-clamp, 20 minutes after the release of the cross-clamp, after CPB, and 2 hours postoperatively. There were no endotoxins in any of the samples before CPB, but it was detected after CPB in both groups. The endotoxin levels were significantly higher in group 1 than in group 2. The present study suggests that when hypothermia is the technique of choice, the deleterious effects of endotoxemia on patients with comorbidity must be considered.
The central nervous system (CNS) may communicate with the immune system by direct innervation of lymphoid organs and/or by
neurotransmitters and changes in neuroendocrine functioning and hormone release. The consequences of selective transient changes
in circulating hormones on immune functioning in humans have not yet been studied. To address this problem, the authors evaluated
the lymphoproliferative responses to optimal and suboptimal concentrations of phytohemagglutinin (PHA) and pokeweed mitogen
(PWM) under selective enhancement of circulating growth hormone, prolactin, or norepinephrine. The authors failed to demonstrate
any effect of elevated growth hormone levels after clonidine challenge on the lymphoproliferative response to mitogens. Similarly,
the results did not show any effect of elevated prolactin concentrations induced by domperidone administration on the immune
test. Exposure of volunteers to cold resulted in elevation of plasma norepinephrine levels without changes in growth hormone,
epinephrine, or cortisol secretion. Cold exposure induced elevation of plasma norepinephrine and reduction of the lymphoproliferative
response to the suboptimal dosage of PHA. The reduction was significant 180 and 240 min after exposure. These results are
indicative of a relationship between norepinephrine and immunity.
Acute cold stress is a consistent stimulus to ACTH secretion in rats yet inhibits arginine vasopressin (AVP) in both rats and humans. We have studied the interrelationships of AVP, corticotrophin-releasing factor, and atrial natriuretic factor (ANF) in the hypothalamo-pituitary-adrenal response to acute cold stress in normal humans. Six healthy male volunteers deprived of food and fluid for 6 h, and minimally clothed, were studied in the early afternoon. After a 30-min period at 22 C, subjects were exposed to cold stress (4 C for 30 min), followed by a 30-min equilibration period at 22 C. By the end of the period of cold exposure there was a fall in plasma volume of 7.8 +/- 1.4% (mean +/- SEM), a significant increase in both systolic blood pressure (P = 0.0001) and in plasma norepinephrine level (P = 0.0001), but no change in plasma epinephrine or in plasma ANF. Plasma AVP levels fell significantly (P less than 0.01) to reach a nadir at 5-10 min after cold exposure before returning to baseline levels. A significant fall in plasma cortisol levels occurred during the first 15 min of the baseline period and remained stable thereafter. No significant changes in plasma corticotrophin-releasing factor or ACTH occurred. These results suggest that cold inhibition of AVP release, presumably via afferent baroreceptor pathways, may act to reduce the response of the corticotrophs to a potentially noxious stimulus. Inhibition of AVP and/or ACTH during acute cold exposure are not dependent upon an increase in plasma ANF.
The intensity of cold-induced shivering, quantified by surface electromyography (EMG) and then expressed as a function of the maximal myoelectrical activity (integrated EMG) obtained during a maximum voluntary contraction (MVC), was examined in this study in individuals classified by body fat. In addition, the relationship between shivering and metabolic rate (MR) and the relative contribution of various muscle groups to total heat production were studied. Ten seminude male volunteers, 5 LEAN (less than 11% body fat) and 5 NORM (greater than 15% body fat) were exposed to 10 degrees C air for 2 h. EMG of six muscle groups (pectoralis major, rectus abdominis, rectus femoris, gastrocnemius, biceps brachii, and brachioradialis) was measured and compared with the EMG of each muscle's MVC. A whole body index of shivering, determined from the mass-weighted intensity of shivering of each muscle group, was correlated with MR. After the initial few minutes of exposure, only the pectoralis major, rectus femoris, and biceps brachii continued to increase their intensity of shivering. Shivering intensity was higher in the central muscles, ranging from 5 to 16% of MVC compared with that in the peripheral muscles, which ranged from 1 to 4% of MVC. Shivering intensities were similar in the peripheral muscles for the LEAN and NORM groups, whereas differences occurred in the trunk muscles for the pectoralis major and rectus abdominis. The whole body index of shivering correlated significantly with each individual's increase in MR (r = 0.63-0.97).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of mild hyper- and hypothermic stress on release of selected hormones (somatotropin, noradrenaline, etc.), interferon (IFN), and activity of NK cells in the blood was examined in groups of young males during a 30 min exposure to 39 degrees C and 4 degrees C. A quick release of somatotropin was registered in 44% of examinees in the hyperthermic group, while the persons exposed to 4 degrees C reacted with a release of noradrenaline only. Concurrently, an elevation of NK cell activity was observed both in the subgroup releasing somatotropin after hyperthermic stress and in the group exposed to cold. Since these forms of mild stress did not lead to an appearance of IFN in the serum, the possibility of an NK cell activating effect of somatotropin and/or the adrenal hormones was tested. While the adrenal hormones stimulated the NK cell activity in vitro, no support for a similar role for somatotropin was found.
It is commonly believed that living in polar isolation causes high susceptibility to respiratory illness. At McMurdo Station, a US research base in Antarctica, we tested this belief by comparing, over 36 days (August 31-October 5, 1976), the incidence and severity of respiratory illness in 64 men finishing six months isolation and in 136 men just arrived from the United States. The colds in the two intermingled populations were essentially equivalent. Forty-three per cent of the newcomers and 39% of the wintering group reported colds; symptoms and duration were nearly identical between the two populations. Movement of the colds was slow. The newcomers brought in 31 colds; subsequently, only 52 evenly spaced illnesses arose. Incidence of respiratory illness was twice higher in the smaller living units than in the spacious main dormitory. Two nontypable rhinoviruses, McMurdo 4 and McMurdo 88, were brought in by the new population and were the only viruses isolated. Only McMurdo 88 spread, although more than 65% of the men were antibody-free (less than 1:3) to either agent. McMurdo 88 caused an estimated 60% of antarctic-contracted colds. In brief, this isolated polar group was not especially susceptible to respiratory illness, and virus movement through the group was deliberate.
We have shown that two human monocyte subsets can be isolated from the peripheral blood of healthy donors; these subsets possess different morphological, cytochemical, functional, and in vivo trafficking properties [1]. In this report, these two subsets were further characterized. One subset (intermediate monocytes, IM) has been shown to have significantly lower acid phosphatase activity and total cellular protein content as well as lower peroxidase activity when compared with another subset (regular monocytes, RM). The overall activation status of the two subsets (as determined by their alkaline phosphodiesterase activity) was identical. We also examined the capacity of these subsets to release various cytokines with or without polyriboinosinic and polyribocytidylic acid (Poly I:C) stimulation. There was no appreciable difference in their ability to release interferon (IFN), interleukin 1 (IL-1), and prostaglandin E (PGE) without stimulation, while IM produced slightly, but significantly, higher amounts of colony-stimulating factor (CSF) than RM. The amount of IFN released by IM in response to poly I:C was approximately three times higher than the amount of IFN released by RM. IL-1 was also released in higher amounts by IM than by RM in response to poly I:C. IM were also found to release more CSF than RM in response to poly I:C. In contrast, it was noted that IM secrete significantly less PGE response to poly I:C than do RM. These findings indicate that two purified human monocyte subsets, distinguishable by maturation markers, differ significantly in their ability to release various cytokines after stimulation; this difference may be relevant to potential in vivo roles of these immunoregulatory cells.