Objective To study and explore the relativity of adults HBV vicinal failure and HLA-DR,T cell subset, trace viruses infection. To accumulate date for formulating preventing adult HBV infection prophylactic-therapeutic measures. Methods Select 20 adults randomly who had vaccinated with 10 μg YDV and produced anti-HBS successfully, and another 20 hadn't produced anti-HBs to form two groups-defeated group and contral group. Blood samples from two groups were taken for detecting the level of DR range gene phenotype: T cell subset, white blood cell HLA-DR, HLA-B27, HLA DRB1 * 07, DRB1 * 04, DRB1 * 1001, DQB1 * 0401 and so on. Results The level of CD4-/CD8- is lower in the infection group than in healthy group. But the average level of HLA-DR and HLA-B27 is higher in the infection group. The differences of HLA DRB1 * 07 gene frequency between two groups were significant ( P < 0.05), but the levels of CD3, CD4, CDS, CD7, CD4/CD8 and HLA DRB1 * 04, DRB1 * 1001, DQB1 * 0401 were not significant. Conclusion The failure of HBV vaccination on adults may have relation to HLA-DR, HLA-B27, HLA DRB1 * 07, CD4-/CD8- , etc.

BACKGROUNDPyroptosis is the term for caspase-1-dependent cell death associated with pro-inflammatory cytokines. The role of alveolar macrophage (AM) pyroptosis in the pathogenesis of the acute lung injury and acute respiratory distress syndrome (ALI/ARDS) remains unclear.

METHODSC57BL/6 wild-type mice were assigned to sham, lipopolysaccharide (LPS) + vehicle, LPS + acetyl-tyrosyl-valyl- alanyl-aspartyl-chloromethylketone (Ac-YVAD-CMK) and LPS + Z-Asp-Glu-Val-Asp-fluoromethylketone groups. Mice were given intraperitoneal (IP) injections of LPS. Drugs were IP injected 1 h before LPS administration. Mice were sacrificed 16 h after LPS administration, and AMs were isolated. Western blot analysis for active caspase-1 and cleaved caspase-3, evaluation of lung injury and a cytokine release analysis were performed. AMs were treated with LPS and adenosine triphosphate (ATP); caspase-1-dependent cell death was evaluated using flow cytometry; the apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) pyroptosomes were examined by immunofluorescence.

RESULTSThe expression of activated caspase-1 in AMs was enhanced following LPS challenge compared with the sham group. In the ex vivo study, the caspase-1/propidium iodide-positive cells, caspase-1 specks and ASC pyroptosomes were up-regulated in AMs following LPS/ATP stimulation. The specific caspase-1 inhibitor Ac-YVAD-CMK inhibited the activation of caspase-1 and pyroptotic cell death. Ac-YVAD-CMK also reduced the lung injury, pulmonary edema and total protein in bronchoalveolar lavage fluid (BALF). In addition, Ac-YVAD-CMK significantly inhibited interleukin-α2 (IL-1α2) release both in serum and BALF and reduced the levels of IL-18, tumor necrosis factor-α± (TNF-α±), High Mobility Group Box 1 (HMGB1) in BALF during LPS-induced ALI/ARDS.

CONCLUSIONSThis study reported AM pyroptosis during LPS-induced ALI/ARDS in mice and has demonstrated that Ac-YVAD-CMK can prevent AM-induced pyroptosis and lung injury. These preliminary findings may form the basis for further studies to evaluate this pathway as a target for prevention or reduction of ALI/ARDS.

Acute Lung Injury ; chemically induced ; prevention & control ; Amino Acid Chloromethyl Ketones ; pharmacology ; Animals ; Lipopolysaccharides ; toxicity ; Macrophages, Alveolar ; drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Oligopeptides ; pharmacology ; Pyroptosis ; drug effects