Relationship between leptin levels and suppressed CD4 counts in HIV patients

To examine the relationship between serum leptin levels and suppression of CD4 count in HIV-infected individuals with highly active antiretroviral therapy [HAART]. Thirty seropositive HIV male patients selected from the Infectious Disease Hospital were classified into two groups according to their immunological and virological response to HAART. The first group included 15 male patients with low viral load and low CD4 counts; the second included 15 male patients with low viral load and high CD4 counts. Morning serum leptin and tumor necrosis factor-alpha levels of HIV patients were measured and correlated with fasting serum insulin, Homeostasis Model Assessment for Insulin Resistance [HOMA-IR], HIV viral load and CD4 count. Serum leptin levels were significantly higher in patients with high CD4 counts than in patients with low CD4 counts [mean serum leptin level 47.3 vs. 10.9 ng/ml, respectively; p < 0.0001]. A positive correlation was observed between serum leptin levels and CD4 counts [r = 0.697; p < 0.0001]; positive correlations were also seen between leptin levels and fasting serum insulin and HOMA-IR [r = 0.633, p < 0.0001, and r = 0.537, p < 0.003, respectively]. Serum leptin level was higher in HIV patients with high CD4 count and correlated with fasting serum insulin and HOMA-IR, thereby indicating that HAART treatment could lead to decreased levels of leptin in HIV patients, which might lead to impaired immunological recovery

Asthma during pregnancy: an immunologic perspective

Asthma is one of the most common medical conditions to complicate pregnancy and represents a significant public health issue. Increased maternal complications and adverse fetal outcomes are associated with asthma during pregnancy. Since asthma can adversely affect the outcome of pregnancy, it is important for us to understand the mechanisms underlying asthma during pregnancy. In general, asthma is characterized by an up-regulated systemic production of T-helper 2 [Th2] cytokines. Pregnancy also brings about changes in maternal immune status making it polarized towards the Th2 phenotype. Based on these considerations, we hypothesize that pregnancy-induced immune alterations may modify allergic mechanisms of asthma and that systemic Th2 cytokine and chemokine polarization does occur among asthmatics to a greater extent during pregnancy. We suggest that this is associated with exacerbation of asthma during pregnancy. The pathophysiology of asthma during pregnancy and the interrelationship between these two conditions are reviewed here

Disease activity and cytokine production in mitogen-stimulated peripheral blood mononuclear cells from patients with rheumatoid arthritis

To test whether there are differences in the levels and ratios of 6 pro- and 3 anti-inflammatory cytokines produced by mitogen-stimulated peripheral blood mononuclear cells [PBMCs] in rheumatoid arthritis [RA] subjects compared to controls. 79 participants [42 seropositive RA patients and 37 healthy controls] were enrolled in this study. The production levels in mitogen-stimulated PBMCs of the 6 proinflammatory cytokines [IFN-gamma, TNF-alpha, TNF-beta, lL-8, IL-17, IL-18] and 3 anti-inflammatory cytokines [IL-4, IL-10, IL13] were assayed by ELISA using kits obtained from Immunotech SA. The ratios of pro- to anti-inflammatory cytokines were calculated for all participants. There were significantly elevated levels of IL-8 and IL-10, and reduced levels of IFN-gamma, IL4, and IL-17 in mitogen-stimulated PBMC culture supernatants of RA subjects compared to controls. Of the 18 pro-/anti-inflammatory cytokine ratios, 3 ratios [TNF-alpha/lL13, IL-8/lL-4 and IL-8/lL-13] were significantly higher in RA patients compared to controls; and 6 were higher in controls [IFN-gamma/IL-4; IFN-gamma/IL-10; IFN-gamma/lL-13; TNF-beta/IL10; IL-17/IL-10; IL-18/IL-10]. Activated PBMCs of RA patients, regardless of disease activity, showed higher-level production of IL-8 and IL-10 compared to controls; lower-level production of IFN-gamma, IL-4, and lL-17; and elevated ratios of TNF-alpha/lL-13, IL-8/1L-4 and IL-8/lL-13

role for the immune system in the etiology of pre-eclampsia

Pre-eclampsia [PE] is a common and perhaps the most dangerous complication of pregnancy, causing maternal and perinatal illness or even death of the mother and infant. PE is a multisystem disorder usually associated with raised blood pressure and proteinuria, with a range of other complications in the mother such as oliguria, thrombocytopenia, pulmonary edema or elevated liver enzymes. The fetal syndrome includes adverse placental / fetal outcomes in addition to suspected abruption placentae, intrauterine growth restriction, oligohydramnios and absent or reversed umbilical artery end diastolic flow. PE has been generally viewed as a mysterious disease as its etiology has been unexplained for a long time and is in fact often referred to as "a disease of theories". However, there is now sufficient research data to indicate that the basic cause of the various maternal symptoms of PE is a generalized dysfunction of maternal endothelium and there is reason to believe that generalized endothelial dysfunction appears to be a part of a systemic inflammatory response that involves maternal leukocytes. This review presents a unifying model for the etiology of preeclampsia in which the immune system plays a significant role; inadequate trophoblast invasion of spiral arteries initiates ischemia and hypoxia in the placenta resulting in increased release of trophoblast microparticles and then increased induction of maternal pro-inflammatory cytokines and the activation of maternal endothelial cells. This results in systemic, diffuse endothelial cell dysfunction which appears to be the fundamental pathophysiological feature of this syndrome

immune system in pregnancy: friend or foe?

Pregnancy is an intriguing immunological paradox; how does an allogeneic fetus survive despite a potentially antagonistic maternal immune system, while tissue allografts succumb to rapid immunological rejection? While several hypothetical models have been proposed in the last five decades to explain the immunological success of pregnancy, the model that has survived the test of experimentation is the one that proposes a state of immunomodulation during pregnancy. Several factors appear to prevent the rejection of the fetus. Yet, pregnancy can be compromised by a variety of complications such as recurrent spontaneous miscarriage, preeclampsia and preterm delivery. Research in the field of immunology of pregnancy has opened up the possibility of cellular immune effectors that might underlie these pregnancy complications. Particularly interesting are the effects that pro-inflammatory andanti-inflammatory cytokines have on the conceptus and thus on the success and failure of pregnancy. This review focuses on the association between some cytokines and successful pregnancy on the one hand, and between other cytokines and complications of pregnancy as also the possible pathways of effector function of cytokines in pregnancy loss. This review proceeds to discuss the therapeutic redirection of cytokine profilestowards one that is favorable to the success of pregnancy

Principles of autoimmunity: part II - modes of autoimmune damage

This is Part II of the article Principles of autoimmunity. Part I [pp. 22.25] and Part II are treated as a single CME/CPD article. Readers who study it, answer the questions related to it on page 29, and send a copy of the Answer Sheet [page 54] to the CME Center of KIMS become eligible for 1 CME/CPD credit in Catrgory 1 in the MPC Program of KIMS. To claim credit, the reader has to be registered in the MPC Program, the answer sheet should be received by the CME Center before 31[st] May 2007, and all questions should have been attempted. Readers would then receive a certificate from the CME Center indicating the credit data

immunology of unexplained recurrent spontaneous abortion: Cytokines as key mediators

Spontaneous abortion is one of the most common complications of pregnancy. Recurrent spontaneous abortion [RSA], defined as the occurrence of three consecutive abortions, occurs due to several identifiable causes such as anatomic, genetic, endocrinologic and infectious etiologies, but a substantial proportion of RSA, up to 50-60%, are due to unexplained or unknown etiologies. Of the various humoral immune etiologies that have been investigated, only anti-phospholipid antibodies have been confirmed as being etiologic factors, but that too, in a small proportion of the cases of RSA. Cellular immune effectors and cytokines have been the focus of intense investigation recently, and it appears that certain cytokines may be beneficial to pregnancy, while some are actually antagonistic to pregnancy. This article reviews recent observations on the association between cytokines and unexplained recurrent spontaneous abortion. Evidence from studies on murine and human pregnancy points to a strong association between maternal Th2-type immunity and successful pregnancy on the one hand and between Th1-type immune reactivity and pregnancy loss on the other. While there is a paucity of data from human pregnancy indicating that Th1-type immune effectors actually lead to pregnancy, it is difficult to ignore the compelling evidence linking inappropriate Th1-type immunity to pregnancy loss. Th2-type immunity may play protective roles during pregnancy, hence the nexus between a Th2 shift and successful pregnancy. This article examines these associations and discusses possible mechanisms underlying immunologically- mediated pregnancy failure