Reduced immune responses to an aseptic inflammation in mice with congestive heart failure.

We previously found that mice with congestive heart failure (CHF) were anemic, had decreased bone marrow haematopoiesis and functionally impaired neutrophilic granulocytes despite normal blood concentrations of these cells. We now asked if CHF-mice could mount an adequate immune response when challenged with an acute inflammation. A postinfarction heart failure was induced in mice. Six weeks later the mice had developed CHF. At that time a sterile peritonitis was induced by injection of a casein digest. Five hours after this injection a marked neutrophilia had developed. Specimens were then obtained from peritoneal washings, bone marrow and blood. Total bone marrow cell numbers were halved in CHF-peritonitis mice compared with sham-peritonitis mice. Bone marrow colony-forming cell numbers in CHF-peritonitis mice were only 14% of those in sham-peritonitis mice. The mobilization of leucocytes to the blood was much lower in CHF-peritonitis mice than in sham-peritonitis mice (5.6 vs. 8.1 million cells/mL), as was the peritoneal influx of these cells (1.6 vs. 4.1 million cells). A profound decline (>50%) in the functional activity, determined with various in vitro assays, was evident for both neutrophilic granulocytes and lymphocytes from CHF-peritonitis mice. Heart failure after myocardial infarction in mice may severely compromise their ability to combat an inflammatory challenge. Copyright Blackwell Munksgaard 2005.