[Lipopolysaccharide (LPS) induced pulmonary inflammatory response and effects of TNF in immunocompromised host (ICH)].

OBJECTIVE

To investigate the pulmonary inflammatory response and TNF-mediated effects in ICH.

METHODS

ICH models of guinea pigs were induced successfully by receiving daily intraperitoneal injections of cyclophosphamide (15mg.kg-1.d-1) plus daily subcutaneous injection of cortisone acetate (100mg.kg-1.d-1) for a total of 7 consecutive days. On the day after the final dose of drugs, guinea pigs were challenged intratracheally with LPS (200 micrograms/animal) and were lavaged before and 1, 3, 5, 8, 24 hours after challenged, respectively.

RESULTS

Five hours after LPS challenged, total counts of bronchoalveolar fluid (BALF) cells and the proportion of PMN increased significantly. Although the counts of both PAM and PMN increased, the proportion of PAM decreased gradually accompanied by increase of the proportion of PMNs. Hematoxylin eosin stained lung sections after challenged with LPS showed an acute intraalveolar inflammatory response. After intra-tracheal injection of LPS, the TNF level in BALF progressively increased. Both the TNF level and PMN count started to increase at 1 hour after LPS challenge, peaked at 5 hours. The TNF level in serum did not increase markedly after intratracheal injection of LPS. In the development of an inflammatory response, a large amount of TNF were released in BALF, the level of TNF in BALF was closely matched the influx of PMN.

CONCLUSIONS

The data suggested that TNF was one of the cytokines which mediated influx of PMNs and inflammation. High level of TNF released in BALF of ICH could induce the lung injury. The systemic inflammatory response of ICH was involving immunosuppressed state after intratracheal injection of LPS, however, strong intraalveolar inflammatory response still occurred, which reflected the phenomenon of "compartmentalization" in inflammatory response.