Effects of testosterone on blood leukocytes inPlasmodium berghei-infected mice

Kamis, A. B.; Ibrahim, Jalal

doi:10.1007/bf00930957

Cited by 33 publications

(21 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Considering the immunosuppressive properties of androgens on both humoral and cell-mediated immunities (Olsen and Kovacs 1996), and the major role that testosterone plays in susceptibility to malaria and in the self-healing ability of male mice (Wunderlich et al 1988(Wunderlich et al , 1993Kamis and Ibrahim 1989;Benten et al 1992Benten et al , 1997, the plasma testosterone decrease at 35 d.p.i. may help the infected mouse to cope with the Plasmodium proliferation.…”

Section: Discussionmentioning

confidence: 99%

Reduction in testosterone concentration and its effect on the reproductive output of chronic malaria-infected male mice

2004

View full text Add to dashboard Cite

An experimental host-parasite association involving BALB/c male mice infected with Plasmodium chabaudi chabaudi was used in order to investigate the influence of the parasite on the sexual physiology and behavior of infected hosts. Infected males displayed complete courtship behavior leading to ejaculation and sired litters on several occasions. A weekly assay of testosterone and corticosterone plasma concentrations revealed a twofold decrease in the testosterone level at 4 and 5 weeks post-injection, during recrudescence. This imbalance was accompanied by a decrease in the overall duration of the social investigation contacts occurring during courtship and by a reduction in the fertilization rate of the infected animals. These physiological perturbations can be regarded as an adaptive response of the host to the recrudescing parasites, which illustrates the rodents' capacity for regulating the testosterone profiles needed to balance the competing demands of immunity and reproduction.

show abstract

Section: Discussionmentioning

confidence: 99%

Reduction in testosterone concentration and its effect on the reproductive output of chronic malaria-infected male mice

2004

View full text Add to dashboard Cite

show abstract

“…When animals were exposed to an inflammatory bone loss, high testosterone levels aggravated the pathology; associated also with decreased phosphorus and ALP levels, and increase calcium levels. One possible explanation for these findings is that testosterone possesses immunosuppressive properties, as demonstrated by the suppressive effect on leukocyte count on orchiectomized mice and young male rats [38, 39]. Along those same lines, a recently published paper demonstrated that men using anabolic androgenic steroids present with more severe forms of periodontitis and higher prevalence of periodontopathogenic microorganisms, including some species of Candida [40].…”

Section: Discussionmentioning

confidence: 99%

Testosterone Regulates Bone Response to Inflammation

Steffens

Herrera²,

Coimbra

et al. 2014

Horm Metab Res

View full text Add to dashboard Cite

This study evaluated the alveolar bone response to testosterone and the impact of Resolvin D2 (RvD2) on testosterone-induced osteoblast function. For the in vivo characterization, 60 male adult rats were used. Treatments established sub-physiologic (L), normal (N), or supra-physiologic (H) concentrations of testosterone. Forty rats were subjected to orchiectomy; 20 rats received periodical testosterone injections while 20 rats received testicular sham-operation. Four weeks after the surgeries, 10 rats in each group received a subgingival ligature around the lower first molars to induce experimental periodontal inflammation and bone loss. In parallel, osteoblasts were differentiated from neonatal mice calvariae and treated with various doses of testosterone for 48 h. Cell lysates and conditioned media were used for the determination of alkaline phosphatase, osteocalcin, RANKL, and osteoprotegerin. Micro-computed tomography linear analysis demonstrated that bone loss was significantly increased for both L and H groups compared to animals with normal levels of testosterone. Gingival IL-1β expression was increased in the L group (p < 0.05). Ten nM testosterone significantly decreased osteocalcin, RANKL, and OPG levels in osteoblasts; 100 nM significantly increased the RANKL:OPG ratio. RvD2 partially reversed the impact of 10 nM testosterone on osteocalcin, RANKL, and OPG. These findings suggest that both L and H testosterone levels increase inflammatory bone loss in male rats. While low testosterone predominantly increases the inflammatory response, high testosterone promotes a higher osteoblast-derived RANKL:OPG ratio. The proresolving mediator RvD2 ameliorates testosterone-derived downregulation of osteocalcin, RANKL, and OPG in primary murine osteoblasts suggesting a direct role of inflammation in osteoblast function.

show abstract

“…Castration of male mice reduces, whereas exogenous administration of testosterone increases, mortality after infection with P. chabaudi or P. berghei (15,54). The immunosuppressive effects of testosterone may underlie increased susceptibility to Plasmodium infections in males compared to females.…”

mentioning

confidence: 99%

Involvement of Gonadal Steroids and Gamma Interferon in Sex Differences in Response to Blood-Stage Malaria Infection

et al. 2006

View full text Add to dashboard Cite

To examine the hormonal and immunological mechanisms that mediate sex differences in susceptibility to malaria infection, intact and gonadectomized (gdx) C57BL/6 mice were inoculated with Plasmodium chabaudi AS-infected erythrocytes, and the responses to infection were monitored. In addition to reduced mortality, intact females recovered from infection-induced weigh loss and anemia faster than intact males. Expression microarrays and real-time reverse transcription-PCR revealed that gonadally intact females exhibited higher expression of interleukin-10 (IL-10), IL-15R␣, IL-12R␤, Gadd45␥, gamma interferon (IFN-␥), CCL3, CXCL10, CCR5, and several IFN-inducible genes in white blood cells and produced more IFN-␥ than did intact males and gdx females, with these differences being most pronounced during peak parasitemia. Intact females also had higher anti-P. chabaudi immunoglobulin G (IgG) and IgG1 responses than either intact males or gdx females. To further examine the effector mechanisms mediating sex differences in response to P. chabaudi infection, responses to infection were compared among male and female wild-type (WT), T-cell-deficient (TCR␤␦ ؊/؊ ), B-cell-deficient (MT), combined T-and B-cell-deficient (RAG1), and IFN-␥ knockout (IFN-␥ ؊/؊ ) mice. Males were 3.5 times more likely to die from malaria infection than females, with these differences being most pronounced among TCR␤␦ ؊/؊ , MT, and RAG1 mice. Male mice also exhibited more severe weight loss, anemia, and hypothermia, and higher peak parasitemia than females during infection, with WT, RAG1, TCR␤␦ ؊/؊ , and MT mice exhibiting the most pronounced sexual dimorphism. The absence of IFN-␥ reduced the sex difference in mortality and was more detrimental to females than males. These data suggest that differential transcription and translation of IFN-␥, that is influenced by estrogens, may mediate sex differences in response to malaria.Males are more susceptible to many protozoan infections than females and field and laboratory studies link increased susceptibility to infection with circulating steroid hormones (17,18,39). One genus of protozoan parasites that causes a pronounced sexual dimorphism in vertebrate hosts is Plasmodium. Among humans, although the incidence of infection is often similar between the sexes (see references 51 and 52), sex differences in the intensity of infection are reported in which men have higher parasitemia than women (23, 32, 52). The observation that P. falciparum (i.e., a human malaria parasite) density increases at puberty in men, but not in women, suggests that circulating sex steroids may influence this outcome (23).Studies of rodent malarias have confirmed that males are more likely to die after blood-stage malaria infection than are females (2,3,(54)(55)(56)

show abstract

Effects of testosterone on blood leukocytes inPlasmodium berghei-infected mice

Cited by 33 publications

References 7 publications

Reduction in testosterone concentration and its effect on the reproductive output of chronic malaria-infected male mice

Reduction in testosterone concentration and its effect on the reproductive output of chronic malaria-infected male mice

Testosterone Regulates Bone Response to Inflammation

Involvement of Gonadal Steroids and Gamma Interferon in Sex Differences in Response to Blood-Stage Malaria Infection

Contact Info

Product

Resources

About