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Background Immunosuppression has been described as a consequence of brain injury and infection by different mechanisms. Angiostrongylus cantonensis can cause injury to the central nervous system and eosinophilic meningitis to human. Both T cell and B cell immunity play an essential role in the resistance of the infection. However, whether brain injury caused by A. cantonensis infection can lead to immunosuppression is not clear. Therefore, the present study sought to observe the alteration of immune responses in mice infected with A. cantonensis . Methods Mice were infected with 20 third-stage A. cantonensis larvae. The messenger RNA (mRNA) expression of inflammatory mediators in brain tissues was observed by qRT-PCR. Cell surface markers including CD3, CD4, CD8, CD19, B220, 7-AAD, annexin-V, IgM, AA4.1, and CD23 were evaluated by using flow cytometry. The immune functions of T and B lymphocytes were detected upon stimulation by ConA and antibody responses to a nonself antigen OVA, respectively. Activation of the hypothalamic-pituitary-adrenal axis was evaluated by analyzing the concentration of plasma corticosterone and levels of mRNA for corticotropin-releasing hormone, tyrosine hydroxylase, and c-fos. Results A. cantonensis infection results in obvious immunosuppression evidenced as progressive spleen and thymus atrophy and significant decrease in the number of lymphocyte subsets including B cells, CD3 + T cells, CD4 + T cells, and CD8 + T cells, as well as reduced T cell proliferation at 21 days post-infection and antibody reaction to exogenous protein after infection. However, the sharp decrease of splenic and thymic cells was not due to cell apoptosis but to B cell genesis cessation and impairing thymocyte development. In addition, helminthicide treatment with albendazole on infected mice at 7 days post-infection could prevent immunosuppressive symptoms. Importantly, infected mice displayed hypothalamic-pituitary-adrenal axis activation, with peak responses occurring at 16 days post-infection, and glucocorticoid receptor antagonist could partially restore the infection-induced cessation of B cell genesis. Conclusions Brain injury caused by A. cantonensis infection, like that of brain stroke and trauma, enhanced endogenous corticosteroid activity, resulting in peripheral immunosuppression.

The mechanisms underlying the domestication process have already been well explained. Starting with Belyaev’s pioneering experiment on silver foxes, which showed that selection for tameness (reduced fear response, changes in the ‘hypothalamic-pituitary-adrenal system’—HPA axis) leads to destabilisation of the regulatory systems that control morphological and behavioural development, resulting in the changes characteristic of the domestication syndrome. Later, the thyroid rhythm hypothesis and the neural crest cell (NCC) hypothesis provided additional explanations. Recently, the parasite-mediated domestication hypothesis (PMD) has been proposed, suggesting an important role of endoparasites in the domestication process. Since parasites either directly or indirectly affect all mechanisms underlying the domestication syndrome (HPA, thyroid, NCC), the PMD proposes that they may be an important trigger of domestication. PMD can be tested either experimentally or comparatively. One of the basic assumptions of PMD is that parasite-susceptible, genetically less resistant/more tolerant wild animals were originally domesticated and that the susceptibility to parasites has been passed on to today’s domestic animals. This can be verified primarily by comparing the parasite susceptibility of existing wild and domestic populations of the same species. We, therefore, followed a systematic comparative approach by analysing the parasite load in wild boar (WB) and free-ranging domestic pig (DP) populations from a comparable environment in a geographically close area. Fresh faeces from WB and DP populations, one each from Slovenia (SI) and Croatia (HR), were sampled. A total of 59 individual faecal samples were collected (SI: 12 WB, 20 DP; HR: 14 WB, 13 DP). Parasitological diagnostics were carried out using the sedimentation and floatation method. Five different taxa were found in WB and seven in DP. Three parasite taxa were found exclusively in DP ( Cystoisospora suis , Trichuris sp., Balantidium coli ), and one ( Strongyloides sp.) only in WB. Of the parasites found in both cohorts, strongyles/ Oesophagostomum sp. were significantly more abundant in DP, while Eimeria sp. was found in equal amounts in both (but in HR only in WB). According to the preliminary study presented here, there is evidence to support the PMD baselines in the wild boar—domestic pig association. However, we cannot draw a definitive conclusion as there are many aspects that may bias the interpretation based on parasite load alone, which are also discussed here. Therefore, comparative studies should be supported by a more focussed methodology, including an experimental approach.

The course of Strongyloides stercoralis infection is usually asymptomatic with a low discharge of rhabditoid larva in feces. However, the deleterious effects of alcohol consumption seem to enhance the susceptibility to infection, as shown by a fivefold higher strongyloidiasis frequency in alcoholics than in nonalcoholics. Moreover, the association between S. stercoralis infection and alcoholism presents a risk for hyperinfection and severe strongyloidiasis. There are several possible mechanisms for the disruption of the host-parasite equilibrium in ethanol-addicted patients with chronic strongyloidiasis. One explanation is that chronic ethanol intake stimulates the hypothalamic-pituitary-adrenal (HPA) axis to produce excessive levels of endogenous cortisol, which in turn can lead to a deficiency in type 2 T helper cells (Th2) protective response, and also to mimic the parasite hormone ecdysone, which promotes the transformation of rhabditiform larvae to filariform larvae, leading to autoinfection. Therefore, when untreated, alcoholic patients are continuously infected by this autoinfection mechanism. Thus, the early diagnosis of strongyloidiasis and treatment can prevent serious forms of hyperinfection in ethanol abusers.

Human malaria, caused by Plasmodium parasites, is a fatal disease that disrupts the host’s physiological balance and affects the neuroendocrine system. This review explores how malaria influences and is influenced by hormones. Malaria activates the Hypothalamus-Pituitary-Adrenal axis, leading to increased cortisol, aldosterone, and epinephrine. Cortisol, while reducing inflammation, aids parasite survival, whereas epinephrine helps manage hypoglycemia. The Hypothalamus-Pituitary-Gonad and Hypothalamus-Pituitary-Thyroid axes are also impacted, resulting in lower sex and thyroid hormone levels. Malaria disrupts the renin-angiotensin-aldosterone system (RAAS), causing higher angiotensin-II and aldosterone levels, contributing to edema, hyponatremia and hypertension. Malaria-induced anemia is exacerbated by increased hepcidin, which impairs iron absorption, reducing both iron availability for the parasite and red blood cell formation, despite elevated erythropoietin. Hypoglycemia is common due to decreased glucose production and hyperinsulinemia, although some cases show hyperglycemia due to stress hormones and inflammation. Hypocalcemia, and hypophosphatemia are associated with low Vitamin D3 and parathyroid hormone but high calcitonin. Hormones such as DHEA, melatonin, PTH, Vitamin D3, hepcidin, progesterone, and erythropoietin protects against malaria. Furthermore, synthetic analogs, receptor agonists and antagonists or mimics of hormones like DHEA, melatonin, serotonin, PTH, vitamin D3, estrogen, progesterone, angiotensin, and somatostatin are being explored as potential antimalarial treatments or adjunct therapies. Additionally, hormones like leptin and PCT are being studied as probable markers of malaria infection.

Extravagant ornaments used as social signals evolved to advertise their bearers' quality. The Immunocompetence Handicap Hypothesis proposes that testosterone-dependent ornaments reliably signal health and parasite resistance; however, empirical studies have shown mixed support. Alternatively, immune function and parasite resistance may be indirectly or directly related to glucocorticoid stress hormones. We propose that an understanding of the interplay between the individual and its environment, particularly how they cope with stressors, is crucial for understanding the honesty of social signals. We analyzed corticosterone deposited in growing feathers as an integrated measure of hypothalamic-pituitary-adrenal activity in a wild territorial bird, the red grouse Lagopus lagopus scoticus. We manipulated two key, interrelated components, parasites and testosterone, which influence both ornamentation and fitness. Birds were initially purged of parasites, and later challenged with parasites or not, while at the same time being given testosterone or control implants, using a factorial experimental design. At the treatment level, testosterone enhanced ornamentation, while parasites reduced it, but only in males not implanted with testosterone. Among individuals, the degree to which both parasites and testosterone had an effect was strongly dependent on the amount of corticosterone in the feather grown during the experiment. The more stressors birds had experienced (i.e., higher corticosterone), the more parasites developed, and the less testosterone enhanced ornamentation. With this unique focus on the individual, and a novel, integrative, measure of response to stressors, we show that ornamentation is ultimately a product of the cumulative physiological response to environmental challenges. These findings lead toward a more realistic concept of honesty in signaling as well as a broader discussion of the concept of stress.

Background The hypothalamo-pituitary-adrenal (HPA) axis modulates the inflammatory response during sepsis. Macrophage migration inhibitory factor (MIF), which counteracts the anti-inflammatory activity of glucocorticoid (GC), is one of the mediators of the development of inflammation. An inflammatory imbalance involving GC and MIF might be the cause or result of adrenal insufficiency. Our objective was to clarify the relationship between serum MIF and adrenal function in the HPA axis of sepsis patients using the adrenocorticotropic hormone (ACTH) stimulation test. Methods An observational study was performed in a university intensive care unit over a two-year period. Of 64 consecutive sepsis patients, 41 were enrolled. The enrolled patients underwent an ACTH stimulation test within 24 h of the diagnosis of severe sepsis or septic shock. Clinical and laboratory parameters, including serum MIF and cortisol, were measured. Results Based on their responses to the ACTH stimulation test, the patients were divided into a normal adrenal response (NAR) group (n = 22) and an adrenal insufficiency (AI) group (n = 19). The AI group had significantly more septic shock patients and higher prothrombin time ratios, serum MIF, and baseline cortisol than did the NAR group ( P < 0.05). Serum MIF correlated significantly with the SOFA (Sequential Organ Failure Assessment) score, prothrombin time ratio, and delta max cortisol, which is maximum increment of serum cortisol concentration after ACTH stimulation test (rs = 0.414, 0.355, and -0.49, respectively, P < 0.05). Serum MIF also correlated significantly with the delta max cortisol/albumin ratio (rs = -0.501, P = 0.001). Receiver operating characteristic curve analysis identified the threshold serum MIF concentration (19.5 ng/mL, P = 0.01) that segregated patients into the NAR and AI groups. Conclusions The inverse correlation between serum MIF and delta max cortisol or the delta max cortisol/albumin ratio suggests that high serum MIF reflects an insufficient adrenal response in the HPA axis. Serum MIF could be a valuable clinical marker of adrenal insufficiency in sepsis patients.

The effects of in vitro treatment of cercariae, schistosomula, and adult worms of Schistosoma mansoni with 4 hypothalamic–pituitary–adrenal (HPA) axis hormones are described. Dehydroepiandrosterone (DHEA) had the strongest effect on viability. Cercariae were more susceptible to this hormone than schistosomula and adults. Mechanically transformed schistosomula showed 100% mortality (determined microscopically by progressive internal disorganization, development of lucent areas in the cytoplasm, and progressive loss of motility) after 48 hr, whereas physiologically induced schistosomula were more resistant, maintaining viability for up to 5 days of exposure. Males were considerably less sensitive than females to the lethal action of DHEA. When adult worms were paired, DHEA lethality was markedly reduced, with viability beginning to decrease only after 4 days in culture. Cortisol reduced the viability of each of the stages tested about equally. Corticotropin-releasing hormone (CRH) and adrenocorticotropin (ACTH) did not affect the viability of any stage. DHEA and cortisol significantly inhibited in vitro oviposition, whereas CRH and ACTH did not. DHEA and cortisol exerted their effects on schistosome viability and oviposition in a concentration-dependent manner. These results suggest possible new avenues for the control of schistosomiasis.

Baboons with primary or secondary exposure to Schistosoma mansoni were compared with each other over a 12-week infection period and with baseline values obtained from uninfected baboons with respect to serum levels of the hypothalamic-pituitary-adrenal (HPA) axis hormones—corticotropin-releasing hormone, adrenocorticotropic hormone, dehydroepiandros-terone sulfate (DHEA-S), and cortisol. Baboons with primary infections, when worm recovery and oviposition rates were high and hepatic schistosome egg granulomas were large, had decreasing levels of these hormones as infection progressed, compared with both uninfected and reexposed baboons. The most reduced hormone level was that of DHEA-S. Reduction of DHEA-S and cortisol levels also occurred in primary murine infections. Reexposedbaboons with low worm recovery and oviposition rates and small (modulated) hepatic granulomas showed the opposite pattern: HPA axis hormone levels were maintained at, or exceeded, the baseline values of uninfected baboons. These results suggest that HPA axis hormones may play a role in regulating the establishment, maturation, and oviposition of schistosomes and the progression of schistosomiasis.