No abstract
Several lines of evidence indicate sexual dimorphism in the immune response. We explored gender differences in phagocytosis by neutrophils (PMNs), CD11b/c expression, generation of cytokine-induced neutrophil chemoattractant (CINC) and the influence of developmental stages on some of these parameters. Phagocytosis by PMNs of reproductive female rats was not suppressed by anesthesia and surgery as it was in age-matched males. The phagocytic response to an endotoxir (ET) challenge was also higher in PMNs of reproductive females than in males or in prereproductive or postreproductive females. CINC generation in reproductive females was lower than in age-matched males. Phagocytosis in saline-treated postreproductive females was reduced compared to reproductive and prereproductive females, but was not different from adult males. CD11b/c expression was greater in PMNs of saline treated postreproductive females, than in reproductive or prereproductive animals, but an ET challenge upregulated CD11b/c expression to the same level in all three groups. No gender difference was observed in this parameter. These data indicate that in terms of phagocytosis PMNs of reproductive female rats are more resistant to the effects of anesthesia and surgery and respond to an ET challenge more vigorously than cells of age-matched males. CINC generation in adult rats is also gender dependent. The developmental stages in females modulate phagocytosis and beta 2-integrin expression in PMNs.
We consider models of heavy fermions in the strong coupling or local moment limit and include phonon degrees of freedom on the conduction electrons. Due to the large mass or low coherence temperature of the heavy fermion state, it is shown that such a regime is dominated by vertex corrections which leads to the complete failure of the Migdal theorem. Even at weak electron-phonon couplings, binding of the conduction electrons competes with the Kondo effect and substantially reduces the coherence temperature, ultimately leading to the Kondo breakdown. Those results are obtained using a combination of the slave boson method and Migdal-Eliashberg approximation as well as the dynamical mean-field theory approximation.Comment: 13 pages, 19 figures; added Ref.7 and comment on the scenario in which phonons couple to the f orbital
Neutrophil accumulation in tissue is a hallmark of inflammation and is associated with a variety of pathological conditions. In bacterial infection neutrophils are selectively attracted in large numbers to phagocytose and kill invading microorganisms. However, activated neutrophils can also cause injury to tissues. To investigate functional alterations in liver recruited neutrophils (PMNs), we studied the functional characteristics of circulating blood and liver sequestered PMNs in terms of host defense mechanisms, such as nitric oxide (NO) and superoxide (SO) generation, beta 2 integrin expression, phagocytosis, and eicosanoid profile. Cells were isolated from rats infused with a nonlethal dose (320 micrograms/kg) of E. coli endotoxin (ET) or pyrogen-free saline for 90 min. Liver PMNs produced significantly more NO both in the absence and in the presence of an in vitro endotoxin challenge than did blood PMNs. No significant difference was observed in phorbol myristate acetate-stimulated SO generation. Endotoxin infusion significantly up-regulated the expression of CD11b/c in circulating and even more so in liver PMNs. Phagocytosis was significantly enhanced by in vivo ET treatment in blood PMNs, and liver PMNs showed even greater phagocytic activity than blood PMNs or Kupffer cells. The percent distribution of prostaglandins D2 and E2 of total 14C-eicosanoids was significantly higher and that of thromboxane B2 and 5-, 12-, and 15-HETEs was significantly lower in liver than in blood PMNs. Our study demonstrates several functional differences between liver-recruited and circulating PMNs in an acute endotoxic model. The implications of altered neutrophil function may extend to mechanisms of host defense and hepatotoxicity associated with sepsis and endotoxemia.
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