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Biomedical subjects

K Granfors

Publications and source records attributed to K Granfors.

At least 55 records · Page 3Linked to original sources
PubMed1996

Expression of MHC class II molecules on human monocytes is regulated independently from each other after phagocytosis of bacteria.

Reactive arthritis is usually self-limiting polyarthritis which develops in HLA-B27 positive individuals after certain gastrointestinal or urogenital infections. The pathogenesis of reactive arthritis is unknown but T cells seem to have a crucial role. Most of the antigen-specific T cells isolated from the synovial fluid have been MHC class II restricted. The role of antigen presentation in the pathogenesis of reactive arthritis has been studied relatively little. In this work the authors studied the effect of arthritis-triggering bacterium (Yersinia enterocolitica O:3) on the expression of MHC class II molecules on human monocytes and found that the expression of different MHC class II molecules was regulated independently from each other in half of the individuals after certain incubation periods. In these cases the expression of HLA-DP was parallel to the expression of HLA-DQ, while HLA-DR expression went to the opposite direction or did not change at all. No difference between HLA-B27 negative and HLA-B27 positive healthy individuals was seen. The authors conclude that independent regulation of the expression of different MHC class II antigens on antigen-presenting cells is a more common phenomenon than usually thought.

Antibodies, Monoclonal↗
PubMed1996

Similarly increased serum IgA1 and IgA2 subclass antibody levels against Klebsiella pneumoniae bacteria in ankylosing spondylitis patients with/without extra-articular features.

IgA1 and IgA2 subclass serum antibodies against whole Klebsiella pneumoniae bacteria were studied earlier in the sera of 98 patients with ankylosing spondylitis (AS) and in 100 healthy blood donors by enzyme immunoassay. In this study, the patients were divided into groups according to the clinical picture, i.e., the presence or absence of iritis and enthesitis. The previous findings of increased IgA1 and IgA2 subclass antibody levels against K. pneumoniae in AS patients when compared to the healthy controls were not specifically associated with any single AS patient group in the present study, but instead were similarly seen in all patient groups with/without extra-articular features. This is in line with the previous studies suggesting a role for K. pneumoniae in the pathogenesis of AS.

Adolescent↗
PubMed1996

Survival and degradation of Salmonella enterica serotype Enteritidis in intestinal epithelial cells in vitro.

The survival and fate of Salmonella enterica serotype Enteritidis in Henle-407 human intestinal epithelial cells was investigated during prolonged incubation to evaluate the persistence of causative microbes and the relationship to patients developing reactive arthritis. Most of the bacteria were killed and degraded quite soon after infection of the cells, but there were still live bacteria inside the cells for up to 14 days. These results suggest that in patients developing reactive arthritis the salmonellae could persist in the epithelial cells and spread within the host to the joint and be present there at the time of the inflammatory response. Production of marked amounts of nitric oxide was observed as a novel response to salmonella infection in human intestinal epithelial cells. The present experimental procedure appears to be a suitable model to further investigate host-bacteria interaction in HLA-B27 positive cells from patients developing reactive arthritis.

Arthritis, Reactive↗
PubMed1995

Antibodies to Klebsiella pneumoniae, Escherichia coli and Proteus mirabilis in the sera of patients with axial and peripheral form of ankylosing spondylitis.

IgM, IgG and IgA class serum antibodies against the whole Klebsiella pneumoniae, Escherichia coli and Proteus mirabilis bacteria, as well as against K. pneumoniae and E. coli lipopolysaccharides (LPSs) were studied earlier in two separate patient populations of 99 and 85 patients with ankylosing spondylitis (AS) and in 102 healthy blood donors by enzyme immunoassay. In this study the patients were divided into groups according to the presence or absence of peripheral arthritis. The patients with peripheral type AS had increased levels of IgM and IgA class antibodies against K. pneumoniae, whereas the patients with axial type AS had increased levels of IgG and IgA class antibodies to K. pneumoniae, as well as IgA class antibodies against E. coli and P. mirabilis bacteria. Sulphasalazine treatment decreased the IgM and IgA class antibodies in peripheral AS and IgA class antibodies in axial AS against K. pneumoniae LPS. The antibody levels were also decreased against E. coli and P. mirabilis bacteria in the sera of patients with axial AS. The immunological findings in patients with peripheral and axial form of AS were different from each other and thus may reflect different aetiopathogenetic mechanisms for these two types of AS.

Antibodies, Bacterial↗
PubMed1995

Antibodies to Klebsiella pneumoniae, Escherichia coli and Proteus mirabilis in the sera of ankylosing spondylitis patients with/without iritis and enthesitis.

IgM, IgG and IgA class serum antibodies against the whole Klebsiella pneumoniae, Escherichia coli and Proteus mirabilis bacteria, as well as against K. pneumoniae and E. coli lipopolysaccharides (LPSs) were studied earlier in the sera of 98 patients with ankylosing spondylitis (AS) and in 102 healthy blood donors by enzyme immunoassay. In this study the patients were divided into groups according to the clinical picture, i.e. presence or absence of iritis and enthesitis. The previous major finding of increased IgA class antibody levels against the whole K. pneumoniae bacteria in AS patients when compared to the healthy controls was not specifically associated with any single patient group in the present study. However, the patients with iritis had higher levels of IgA class antibodies to LPS of K. pneumoniae and E. coli when compared to the patients without iritis. In addition, the patients without enthesitis had higher level of IgG class antibodies against whole K. pneumoniae bacteria compared to the patients with enthesitis. The increased IgA class antibody levels against K. pneumoniae and E. coli LPS in AS patients with iritis may reflect an inflammatory process in the gut area. Furthermore, there were certain other differences in the immunological parameters between the AS patients with and without iritis or enthesitis and the possibility that they reflect different mechanisms involved in the disease processes cannot be excluded.

Antibodies, Bacterial↗
PubMed1995

IgA1 and IgA2 subclass antibodies against Klebsiella pneumoniae in the sera of patients with peripheral and axial types of ankylosing spondylitis.

OBJECTIVE: To study further the Klebsiella specific serum antibody response in patients with axial and peripheral types of ankylosing spondylitis (AS). METHODS: IgA1 and IgA2 subclass antibodies to Klebsiella pneumoniae were measured by enzyme linked immunosorbent assay in the sera of 171 patients with axial or peripheral type AS, and in sera of 100 healthy controls. The effect of 26 weeks of sulphasalazine treatment on the antibody levels in the two types of AS was also analysed. RESULTS: K pneumoniae specific antibody levels of both IgA1 and IgA2 subclasses were increased in the sera of patients with AS compared with healthy controls. The increased levels were present in patients with axial and with peripheral AS, and there were no statistically significant differences in the antibody levels between these two groups. Sulphasalazine treatment decreased the Klebsiella specific antibody level of IgA1 subclass in patients with axial AS, but there were no statistically significant changes in the IgA2 subclass, or in the patients with peripheral type AS. CONCLUSIONS: These results agree with earlier published findings suggesting that IgA (especially Klebsiella specific IgA) may have a role in the pathogenetic mechanisms of both peripheral and axial types of AS. In addition, it seems that both IgA1 and IgA2 subclasses are involved in the disease process.

Adolescent↗
PubMed1994

Aberrant binding of lamina propria lymphocytes to vascular endothelium in inflammatory bowel diseases.

BACKGROUND/AIMS: Lymphocyte recirculation between the blood and lymphoid tissues as well as lymphocyte migration into inflammatory sites are controlled by lymphocyte interaction with vascular endothelium. The aim of this study was to compare the endothelial binding mechanisms of lamina propria lymphocytes (LPL) isolated from normal and inflamed bowel. METHODS: Binding of LPL from normal and inflamed (inflammatory bowel disease) bowel to endothelium was studied using an in vitro binding assay. Expression of adhesion molecules on LPL and on mucosal endothelial cells was analyzed by flow cytometry and immunohistochemistry. RESULTS: In inflammatory bowel disease, the selectivity of lymphocyte-endothelial interaction was lost, i.e., immunoblasts bound well not only to mucosal vessels but also to peripheral lymph node venules. The set of homing receptors expressed on mucosal immunoblasts did not directly predict the endothelial binding properties of these cells; e.g., L-selectin-negative blasts adhered well to lymph node vessels using peripheral lymph node-specific endothelial adhesion antigen (PNAd). PNAd was aberrantly expressed in vessels in the inflamed mucosa, where it also mediated LPL binding. CONCLUSIONS: These findings are important in understanding the physiology of lymphocyte homing into the gut and suggest an important role for PNAd in the pathogenesis of inflammatory bowel disease.

Antigens, Surface↗
PubMed1994

IgM, IgA and IgG class serum antibodies against Klebsiella pneumoniae and Escherichia coli lipopolysaccharides in patients with ankylosing spondylitis.

Igm, IgA and IgG class serum antibodies against Klebsiella pneumoniae and Escherichia coli lipopolysaccharides (LPS) were studied by ELISA in two separate AS patient populations of 99 and 81 subjects and in 102 healthy blood donors. In the first patient population increased levels of IgM and IgG class antibodies against K. pneumoniae LPS were observed in patients with active AS. In the population with active AS, increased levels of IgM, IgA and IgG class antibodies against K. pneumoniae LPS and IgA class antibodies against E. coli LPS were observed. Sulphasalazine treatment decreased IgM and IgA class antibody levels significantly against K. pneumoniae LPS and IgM class antibodies against E. coli LPS. These findings suggest that a significant part of the anti-Klebsiella antibodies found in AS patients is directed against the LPS component of Klebsiella.

Antibodies, Bacterial↗
PubMed1994

Reactive arthritis following an outbreak of Salmonella infection in Finland.

The incidence and clinical features of reactive arthritis (ReA) following an outbreak of enteritis caused by Salmonella enterica ssp. enterica serovar 4,5,12:b:-were studied in the autumn of 1992. The outbreak occurred in several municipalities and originated from sprouted mung beans. A questionnaire on extra-enteric manifestations such as joint and eye symptoms was mailed 2 to 5 months after the outbreak to all bacteriologically proven cases. Two hundred and forty-six of the 272 (90%) subjects responded to the questionnaire; 224 (91%) reported having had enterocolitis, 22 (9%) were asymptomatic. Sixteen subjects fulfilled the criteria for ReA, and one had irities only. Thus, the incidence of ReA/iritis after S. enterica was 6.9%. Only four of the 155 (3%) subjects aged less than 16 yr developed ReA, as compared with 12 of the 91 (13%) older patients (P < 0.001). The only patient with iritis was also more than 16 yr old. The joint symptoms were oligoarticular in 10 (63%), monoarticular in five (31%) and polyarticular in one (6%). The most frequently affected joints were the wrists, knees and ankles. Joints of upper extremities only were affected in three (19%), of the lower extremities only in six (37%) and of both in seven (44%) subjects. In the majority of the patients ReA was mild. The joint symptoms persisted for less than 1 month in six, 2 to 6 months in five and more than 6 months in five. Thirteen subjects with ReA/iritis were tissue-typed for HLA; four (33%) had HLA-B27.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Yersinia-specific antibodies in serum and synovial fluid in patients with Yersinia triggered reactive arthritis.

OBJECTIVES: To further evaluate the role of bacterial antigens in triggering inflammation in the joint in patients with reactive arthritis by studying local antibody synthesis in the joint. METHODS: Yersinia-specific antibodies in paired serum and synovial fluid samples from 29 patients with yersinia triggered reactive arthritis were studied using an enzyme linked immunosorbent assay (ELISA), an inhibition ELISA with six monoclonal antibodies against lipopolysaccharide or released proteins of yersinia and immunoblotting. Antibodies of IgM, IgG and IgA classes, as well as antibodies of IgA subclasses and those containing secretory component were measured against the lipopolysaccharide and the sodium dodecyl sulphate extract of whole Yersinia enterocolitica O:3 bacteria. RESULTS: It was shown that yersinia-specific antibodies, as well as antibodies against other microbial antigens (rubella, measles, Bordetella pertussis, tetanus toxoid and Candida albicans) in synovial fluid mirror those in serum by concentration, by specificity and by distribution in classes and subclasses. CONCLUSION: These results do not suggest any strong local antibody production, but indicate that the majority of yersinia antibodies in the synovial fluid are derived from the circulation.

Adolescent↗
PubMed1994

Antibodies to Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis in ankylosing spondylitis: effect of sulfasalazine treatment.

OBJECTIVE: To make a longitudinal study of antibodies to Klebsiella pneumoniae in patients with ankylosing spondylitis (AS) and to assess treatment effects. As a comparison we measured antibodies of 2 other gut associated bacteria, Escherichia coli and Proteus mirabilis. METHODS: In a double blind study in 84 Finnish outpatients with AS before and after 26 weeks' treatment with sulfasalazine or placebo we measured serum antibodies to Klebsiella pneumoniae, E. coli and Proteus mirabilis with ELISA: Serum samples of 100 healthy blood donors served as controls. RESULTS: The levels of IgA class antibodies to all 3 bacteria were statistically significantly higher in the sera of the patients compared to the controls. During sulfasalazine treatment significant decreases were observed in concentrations of the IgA class antibodies to Klebsiella and E. coli whereas only a slight decrease was observed in the concentrations of IgA antibodies to Proteus mirabilis. There were no correlations between the clinical and laboratory results observed with sulfasalazine and decrease in concentrations of IgA class antibodies. CONCLUSION: Our results agree with the role of gut associated lymphoid tissue in the pathogenesis of AS, but do not totally exclude Klebsiella pneumoniae as a specific agent contributing to the development of AS.

Adult↗
PubMed1994

Reactive arthritis: incidence, triggering agents and clinical presentation.

OBJECTIVE: To study the incidence and presenting clinical and microbiological features in subgroups of reactive arthritides. METHODS: In a defined community and during a 2-year period, we studied prospectively patients between 18 and 60 years with onset of suspected reactive arthritis, primarily seen by general practitioners. RESULTS: Annual minimum incidence of Chlamydia induced arthritis (n = 25) was 4.6 and of arthritis triggered by enterobacteria (n = 27) 5.0/100,000 individuals between 18 and 60 years. Triggering infections were asymptomatic in 36 and 26%, respectively. Patients with self-limiting arthritis without identified triggering agents (n = 60, incidence 11.0/100,000) had a normal prevalence of HLA-B27 and a more heterogeneous pattern of arthritis. CONCLUSION: Our epidemiological study confirms suggested high incidence rates of reactive arthritides. Reactive arthritides must be considered in early arthritis, even without symptoms of triggering infections.

Adolescent↗
PubMed1993

Yersinia lipopolysaccharide is modified by human monocytes.

Reactive arthritis is usually self-limiting polyarthritis, which develops after certain gastrointestinal or urogenital tract infections, mostly in susceptible HLA B27-positive individuals. In the pathogenesis of this arthritis, it is probably important that structures of the causative bacteria are found in the affected joints. The structure found in the synovial fluid phagocytes of the patients with reactive arthritis after Yersinia, Salmonella, and Shigella infections has always been lipopolysaccharide (LPS) of the causative bacteria. It has been in a highly processed form but still immunoreactive. To follow the degradation process of LPS, we fed peripheral blood monocytes of healthy blood donors with heat-killed Yersinia enterocolitica O:3 bacteria in vitro and monitored the fate of LPS by immunofluorescence and immunoblotting methods. Heat-killed bacteria were used since Y. enterocolitica O:3 bacteria are able to live inside monocytes in vitro and dividing intracellular bacteria would have made it impossible to monitor the degradation process of LPS with these methods. Both the core region and the O-polysaccharide chain of LPS persisted in cytoplasmic vacuoles and on plasma membrane of monocytes through the 7-day follow-up time. Migration properties of processed LPS in sodium dodecyl sulfate-polyacrylamide gel electrophoresis suggested structural modifications of LPS. We also demonstrated that core epitopes appearing on the surface of Yersinia-fed monocytes on day 4 of incubation were processed intracellularly, suggesting that LPS-containing phagocytes are a constant source of membrane-active LPS in their microenvironment as well as in the joints of arthritic patients.

Antigens, Bacterial↗
PubMed1992

Selective endothelial binding of interleukin-2-dependent human T-cell lines derived from different tissues.

The ability of lymphocytes to recognize and bind to high endothelial venules (HEVs) is essential for lymphocyte migration from the blood into lymphoid tissues and into sites of inflammation. Endothelial cell binding capacity also critically determines the clinical usefulness of T-cell lines and clones in immunotherapy. In the present study, interleukin-2-dependent T-cell lines were derived from the blood, lamina propria of the gut, inflamed synovium, synovial fluid, and peripheral lymph nodes. After 3-8 weeks of culture, the expression of homing-associated molecules and binding to mucosal, synovial, and peripheral lymph node HEVs were analyzed. Cell lines derived from the blood and mucosal sites bound significantly better to mucosal and synovial HEVs than to peripheral lymph node HEVs. Three out of seven synovial T-cell lines showed preferential binding to synovial HEVs, whereas the rest bound almost equally well to synovial and mucosal HEVs. T-cell lines from peripheral lymph nodes bound preferentially to lymph node HEVs despite the lack of L-selectin (the peripheral lymph node homing receptor). Expression of the known homing-associated molecules did not predict the HEV-binding specificity of these lines. Importantly, two cell lines bound well to synovial venules, but poorly, if at all, to mucosal or peripheral lymph node HEVs, supporting the concept that synovial-specific HEV recognition mechanisms exist. In conclusion, the tissue origin of T-cell lines critically determines their selectivity for endothelial cell recognition, and besides the known "homing receptors," other molecules may also mediate tissue-specific HEV-binding of interleukin-2-activated T cells.

Antigens, CD↗
PubMed1992

Yersinia-triggered reactive arthritis. Use of polymerase chain reaction and immunocytochemical staining in the detection of bacterial components from synovial specimens.

OBJECTIVE: To investigate whether microbial DNA is present in synovial specimens from patients with Yersinia-triggered reactive arthritis. METHODS: Synovial specimens from 13 patients with Yersinia enterocolitica O:3-triggered reactive arthritis and from 16 control patients were studied using polymerase chain reaction and immunocytochemical staining techniques. RESULTS: Yersinia chromosomal DNA was not found in any of the synovial specimens from Yersinia-triggered arthritis patients or controls, whereas with immunocytochemical techniques, Yersinia antigens were observed in synovial specimens from all of the patients with Yersinia-triggered reactive arthritis. CONCLUSION: Only stable bacterial degradation products, not whole bacteria, are present at the site of inflammation in Yersinia-triggered reactive arthritis.

Adult↗