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S Nanda

Publications and source records attributed to S Nanda.

72 records · Page 4Linked to original sources
PubMed1983

Secretion of chondrocyte stimulating factor by macrophages as a result of activation with collagen and proteoglycans.

In this study, we have investigated the role of extracellular matrix components of connective tissue, collagen and proteoglycans, in the activation of rabbit macrophages and articular chondrocytes. Addition of type II collagen, in native or denatured form, or proteoglycan subunits, led to the activation of macrophages and release of chondrocyte stimulating factor. Type I collagen, when used at higher concentrations, was also capable of macrophage activation. The conditioned media of activated macrophages induced an increased protease synthesis by chondrocytes. Collagen or proteoglycan subunits did not have any direct stimulatory effect on chondrocytes. Intraperitoneal injections of collagen induced infiltration of macrophages into the peritoneal cavity. Although these macrophages failed to produce significant levels of chondrocyte stimulating factor by themselves, they could be activated in culture with lipopolysaccharides or collagen to produce chondrocyte stimulating factor. The chondrocytes, treated with the conditioned medium of activated macrophages (with lipopolysaccharides or cartilage matrix components), failed to survive in suspension cultures.

Animals↗
PubMed1982

Effects of various anti-inflammatory drugs on type II collagen-induced arthritis in rats.

The effects of some commonly used anti-inflammatory and anti-arthritic drugs on the inflammatory and immunological manifestations of type II collagen-induced arthritis in rats were studied. Among the anti-inflammatory drugs tested at a given dosage (mg/kg/day), benoxaprofen (10), aspirin (25) and indomethacin (3) inhibited the hind paw swelling and anti-type II collagen antibody formation in type II collagen-treated rats. Benoxaprofen also inhibited the delayed type hypersensitivity (DTH) response to type II collagen. Phenylbutazone (30) and fenoprofen (40) partially suppressed the paw swelling, but had no significant effect on humoral and cellular responses. Among the other anti-arthritic drugs, levamisol (25), chloroquine (25) and D-penicillamine significantly suppressed the paw swelling, anti-type II collagen antibody titres and DTH response. Gold chlorophosphene (10) and colchicine (3) had no effect on any of these three parameters. Paramethasone (0.1), cyclophosphamide (1) and azathioprine (10) were very effective when dosed daily, or once (at a different dose) 72 hr prior to immunization with type II collagen.

Animals↗
PubMed1982

Effects of benoxaprofen on the inflammatory, humoral and cellular components of type II collagen-induced arthritis in rats.

The effects of benoxaprofen and some other anti-inflammatory drugs on the inflammatory, cellular, and humoral components of type II collagen-induced arthritis in rats were studied. At the given dosage (mg/kg/day), benoxaprofen (10), aspirin (25), and indomethacin (3) inhibited the hindpaw swelling and development of anti-type II collagen antibodies in collagen-treated rats. Benoxaprofen also inhibited the delayed-type hypersensitivity response to collagen. Phenylbutazone (30) failed to show significant effect on these parameters. The treatment of rats with benoxaprofen throughout the test period or during days 14 to 28 was more effective than the treatment in the initial phases only.

Animals↗
PubMed1981

Release of chondrocyte-stimulating factor by rabbit peritoneal macrophages.

Cultured rabbit peritoneal macrophages, after stimulation with lipopolysaccharides (LPS), produce a factor that induces normal rabbit articular cartilage cells (chondrocytes) to release collagenase and other neutral proteases in their culture medium. The release of the factor as well as the activation of chondrocytes can be significantly inhibited by paramethasone (10(-6) M). Rabbit peripheral blood monocytes produce this factor in smaller quantities. Activation with LPS does not enhance the release of factor any further by these cells. Lymphocytes have no direct effect on the chondrocytic protease synthesis. Furthermore, conditioned medium of activated lymphocytes failed to stimulate monocytes or macrophages in the absence of LPS. The macrophage medium exhibits mitogenic and phytohaemagglutinin-enhancing activity towards thymocytes of C3H/HeJ mice, but not against species-specific rabbit lymphocytes. The lymphocyte-activating factor, derived from a mouse macrophage cell line, P388D1 cells, or from other sources, was unable to stimulate chondrocytic protease secretion. Such specific induction of chondrocytic proteases by a macrophage-derived factor may have an important role in cartilage destruction in arthritic conditions, where synovium is only marginally involved.

Animals↗
PubMed1980

Macrophage factor that induces neutral protease secretion by normal rabbit chondrocytes. Studies of some properties and effects on metabolism of chondrocytes.

Normal rabbit-articular chondrocytes secrete very small amounts of degradative enzymes in culture. Rabbit peritoneal macrophages, when activated with lipopolysaccharides, release a factor in the medium which stimulates the chondrocytes to produce significantly high levels of collagenase and other neutral protease for 2-3 days. The soluble mediator from macrophages appears to be a polypeptide with a molecular weight of 13000-15000 and can be inactivated by short-term treatment with trypsin or pronase. The enzyme-synthesis by chondrocytes can be stimulated to the same extent by repeated addition of the macrophage-medium. The metabolism of chondrocytes is altered due to the presence of this mediator. The cellular proliferation is diminished, while the rates of degradation as well as biosynthesis of the matrix are increased. These studies suggest the possibility that in the conditions such as osteoarthritis, where the synovial cells may not play an active role in cartilage degradation, the proteases can be produced by the cartilage cells themselves after the stimulation by macrophage-derived mediators. These intrinsic enzymes may be responsible for the slow, but progressive degeneration of cartilage tissue.

Animals↗
PubMed1975

Cellular composition of the islets of langerhans in the himalayan toad, Bufo melanostictus (Schneider): a light microscopical study.

The pancreatic islet tissue of Bufo melanostictus, investigated by differential staining techniques, is generally condensed in the anterior and middle regions, and contains distinguishable islets of various size, shape and or irregular configuration. Histologically, 3 distinct cell types have been identified: B, A1 and A2. Various tinctorial characteristics of B cells reveal that they correspond to the insulin producing B-cells of other vertebrates. The A cells are a few in number, some of which definitely show positive argyrophilia (= A1). A few isolated A- and B-cells are found scattered in the exocrine tissue. A conspicuous feature of several B-cells in some specimens of Bufo melanostictus is the presence of vacuoles of varying size.

Animals↗