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Background: Injury induces systemic inflammatory response. The degree of response is proportionate to the trauma.
Methods: Patients with ultrasound-proven gall stones posted for operation were randomized into two groups. Laparoscopic cholecystectomy was performed in one group while the other group underwent conventional cholecystectomy. Peripheral venous blood samples for inflammatory mediators, namely tumour necrosis factor, C-reactive protein, oxygen release from monocytes and polymorphonuclear leucocytes were drawn 1 day before surgery and repeated on the first and third days after surgery. Partial pressure of arterial oxygen was also measured in both groups. Only patients who met selection criteria and had uncomplicated postoperative courses were included in the study.There was a total of 40 patients for the final analysis, 20 in each group.
Results: There was no significant difference (P > 0.1) in age, sex or body mass index in both groups of patients. The level of all of the inflammatory mediators was elevated on the first postoperative day; however, the elevation was significantly less following laparoscopic cholecystectomy compared to conventional cholecystectomy (P < 0.01). Although the values came down on the third postoperative day, they remained above the respective controls. Postoperative hypoxaemia was significantly more in patients of conventional than laparoscopic cholecystectomy (P < 0.001).
Conclusions: Trauma-induced inflammatory response is significantly less following laparoscopic cholecystectomy compared to conventional cholecystectomy. It appears to be related to degree of trauma.

The role of Plasmodium falciparumand blood monocytes in the erythrocyte damage and pathogenesis of anemia has been investigated using two strains of the parasite; one laboratory-established strain (FSJ-M) and one wild, fresh, clinical isolate (PfPGI). Peripheral blood monocyte-induced growth inhibition of the parasites, erythrocyte membrane lipid peroxidation as seen by the formation of lipid peroxide products, and sensitivity to peroxide hemolysis at atmospheric oxygen were evaluated. The growth inhibition of FSJ-M by activated blood monocytes was greater than that of PfPGI. The extent of lipid peroxidation and sensitivity to hemolysis increased significantly as the parasites matured. These adverse effects were more marked following exposure to activated monocytes, especially in synchronized, parasitized RBCs. In addition, uninfected erythrocytes within the PfPGI parasite culture revealed a significant increase in the lipid peroxide formation (P< 0.01) and susceptibility to lysis (P< 0.05) under similar oxidant stress induced by monocytes from normal healthy donors. Furthermore, there was a direct correlation between membrane lipid peroxidation and peroxide hemolysis, both before and after monocyte exposure, suggesting a primary role of membrane peroxidation in red cell lysis. The contribution of intraerythrocytic parasites and nonspecific activation of blood monocytes in the pathophysiology of erythrocyte damage and anemia of P. falciparuminfection is discussed.

An experimental model of carditis has been produced in the rhesus monkey by giving 12 weekly injections of a streptococcal membrane antigen. There was histological evidence of focal myocarditis, subendocardial infiltration with lymphomononuclear cells and in one animal myocardial granuloma formation. No valvular lesions were seen. Humoral immune responses monitored throughout the experiment showed that anti-heart antibodies appeared in circulation after the 2nd injection, attained maximal titres by the 6th injection, and thereafter the titres declined. The anti-membrane antibodies appeared slightly later and these titres kept rising till sacrifice. By the 6th injection there was evidence of complement consumption and appearance of circulating immune complexes. It is concluded that these immunological responses might have a role to play in the pathogenesis of carditis.

Infection with Leishmania donovanileads to activation of liver macrophages. The role of different macrophage populations of liver in this infection is not clearly defined. Thus, the mechanism involved in hepatocyte damage was studied by coculturing hepatocytes with two populations of liver macrophages, the kupffer cells and immigrant macrophages. The results indicated maximum tissue damage at peak infection in both the macrophage populations cocultured with hepatocytes (P < 0.001). Kupffer cell-hepatocyte coculture treated with scavengers of reactive oxygen intermediates failed to inhibit the hepatocyte damage (P > 0.05). But with heparin and phenylmethylsulfonyl fluoride, a sharp decrease in the damage was noticed (P < 0.001). In contrast, immigrant macrophage-hepatocyte coculture showed a significant reduction in tissue damage when treated with both the scavengers of reactive oxygen intermediates and enzyme inhibitors (P < 0.001). Therefore the murine infection with L. donovaniis speculated to involve two distinct subpopulations of liver macrophages with marked differences in morphology and functional capabilities.

To investigate the involvement of immune complexes in the pathogenesis of cerebral malaria, a comparative study between Plasmodium bergheiinfected Swiss albino mice and BALB/c mice was conducted. Rise in parasitemia was found to be same with differences in manifestation of disease and mortality, level of immune complexes and histopathology. Increased parasitized red cells with swelling of endothelial cells in the brain capillaries along with increased levels of circulating immune complexes were observed in the BALB/c mice.

A purified 200-kDa antigenic fraction from Leishmania donovaniaxenic amastigotes was evaluated by ELISA for the detection of antibody response in visceral leishmaniasis (VL) patients, post kala-azar dermal leishmaniasis (PKDL) patients and controls, for the diagnosis of visceral leishmaniasis. A positive antibody response to the 200-kDa amastigote fraction and to Leishmaniaamastigote soluble antigen (LASA) was found in 29 (96·6%) and 30 (100%) confirmed VL patients, respectively, by the use of ELISA. However, only 1 (10%) out of 10 PKDL patients had detectable antibody response to 200-kDa fraction while all the 10 (100%) PKDL patients exhibited an immune response to LASA. Therefore, use of the 200-kDa antigenic fraction for the detection of antibody response in an ELISA follow-up (post treatment) of VL patients may have prognostic significance, and it may also be useful for differentiating active VL and PKDL.