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Biomedical subjects

B K Verma

Publications and source records attributed to B K Verma.

5 recordsLinked to original sources
PubMed1995

Effect of stressful environmental factors upon neonatal immune system.

To examine the effects of stressful environmental conditions upon the immune system of the newborn (neonates), we analyzed the neonatal serum immunoglobulin levels in a total of 67 neonates from tribal families living in a rural community of eastern India. These cases were grouped into three categories, based upon the predominance of one of the three factors being analyzed, and the reasonable absence of the other two factors. The three factors as determined by the prevailing environmental conditions, which were the basis for forming the three groups, were: 1. indoor air pollution; 2. hygienic conditions, and 3. the cohabitation of domesticated animals in the same household as the infants's families. Presence of indoor air pollution or unhygienic conditions resulted in the disturbance and depression of the levels of serum immunoglobulins of different classes. There was no discernible correlation found between the levels of immunoglobulins of different classes from the neonates (except IgM) and the cohabitation of domesticated animals in the same households. However the incidence of GIT and RT infections was higher in all the three experimental groups, as compared to the control group. These results suggest that unfavorable environmental conditions can adversely affect the immune system at neonatal stages, and can increase their susceptibility to subsequent acute or chronic events.

Air Pollution, Indoor↗
PubMed1993

Down-regulation of tumor necrosis factor alpha activity by acute ethanol treatment in human peripheral blood monocytes.

As the most commonly used drug that can modulate both metabolic and immune pathways, ethanol is evaluated in this report as a regulator of tumor necrosis factor alpha (TNF alpha) production in human peripheral blood monocytes (M phi) in combination with a variety of stimuli. While acute ethanol treatment did not induce TNF alpha in M phi, it was a potent down-regulator of M phi TNF alpha production whether induced by the combination of interferon-gamma plus muramyl dipeptide (MDP) (P < 0.001), lipopolysaccharide (LPS) alone (P < 0.01), or interferon-gamma plus LPS. Down-regulation of M phi TNF alpha by ethanol was dose dependent and statistically significant in the biologically relevant, 25-150 mM, ethanol concentration range. We also demonstrate that these ethanol concentrations did not affect M phi viability. TNF alpha down-regulation by ethanol was most effective when ethanol was administered 4 hr prior to MDP stimulation; however, it was also effective--though to a lesser extent--if it was added at the time of MDP stimulation. Furthermore, ethanol also down-regulated TNF alpha production of the in vivo preactivated M phi of trauma patients, which produce hyperelevated levels of TNF alpha. We have previously shown that the majority of posttrauma elevated M phi TNF alpha is produced by the M phi subpopulation expressing high-affinity type I Fc gamma receptors (Fc gamma RI). When the Fc gamma RI cross-linking-stimulated M phi subpopulation was treated with acute ethanol, TNF alpha production was suppressed again both in in vivo preactivated M phi of trauma patients and in M phi of normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1992

Induction of transforming growth factor-beta and prostaglandin E2 production by ethanol in human monocytes.

To test our hypothesis that monocytes (M phi) and their mediators are major contributors to ethanol-related immunodepression, the modulating capacity of acute ethanol treatment was assessed on the production of transforming growth factor-beta (TGF beta) and prostaglandin E2 (PGE2) by human peripheral blood M phi. We demonstrate that acute in vitro treatment of adherent M phi with either 50 or 150 mM ethanol induced a significant increase in the production of TGF beta (P < 0.045 and P < 0.001, respectively). Furthermore, M phi pretreatment with both 50 and 150 mM ethanol augmented TGF beta production in response to subsequent stimulation with the synthetic bacterial analog, muramyl dipeptide (MDP) (P < 0.05 and P < 0.001, respectively). Ethanol also increased TGF beta production in interferon gamma (IFN gamma-activated M phi in response to MDP stimulus (P < 0.05). M phi TGF beta levels, however, were always lower in IFN gamma-activated than in non-IFN gamma-activated M phi after the same stimulation with ethanol plus MDP, suggesting that M phi preactivation by IFN gamma can partially counteract the TGF beta inducing potential of ethanol. Similar to its TGF beta-inducing potential, ethanol (150 mM) had the capacity to induce PGE2 production in adherent human M phi (P < 0.045). However, ethanol failed to augment M phi PGE2 production induced by the PGE2 secretagogue, MDP. TGF beta induction by ethanol was unaffected by the presence of cyclooxygenase inhibitor, suggesting that ethanol-induced M phi TGF beta production does not require M phi PGE2 production. These results indicate that ethanol is a potent inducer for inhibitory M phi mediators, TGF beta and PGE2, and also has the capacity to augment M phi TGF beta production in response to subsequent stimulation. Thus, ethanol-induced elevation of M phi TGF beta and PGE2 production might contribute to decreased T cell proliferation and abnormal M phi functions after alcohol exposure, resulting in a depressed immune response.

Cell Line↗