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J Bacteriol. 2000 Dec;182(24):7067-9.
Intergeneric communication in dental plaque biofilms.

Xie H, Cook GS, Costerton JW, Bruce G, Rose TM, Lamont RJ.

School of Dentistry, Meharry Medical College, Nashville, Tennessee 37208, USA. hxiail.mmc.edu

Dental plaque is a complex biofilm that accretes in a series of discrete steps proceeding from a gram-positive streptococcus-rich biofilm to a structure rich in gram-negative anaerobes. This study investigated information flow between two unrelated plaque bacteria, Streptococcus cristatus and Porphyromonas gingivalis. A surface protein of S. cristatus caused repression of the P. gingivalis fimbrial gene (fimA), as determined by a chromosomal fimA promoter-lacZ reporter construct and by reverse transcription-PCR. Signaling activity was associated with a 59-kDa surface protein of S. cristatus and showed specificity for the fimA gene. Furthermore, P. gingivalis was unable to form biofilm microcolonies with S. cristatus. Thus, S. cristatus is capable of modulating virulence gene expression in P. gingivalis, consequently influencing the development of pathogenic plaque.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11092870&dopt=Abstract

aecom.yu.edu

Infection with Mycobacterium tuberculosis remains a major global health emergency. Although detailed understanding of the molecular events of M. tuberculosis pathogenesis is still limited, recent genetic analyses have implicated specific lipids of the cell envelope as important effectors in M. tuberculosis pathogenesis. We have shown that pcaA, a novel member of a family of M. tuberculosis S-adenosyl methionine (SAM)-dependent methyl transferases, is required for alpha-mycolic acid cyclopropanation and lethal chronic persistent M. tuberculosis infection. To examine the apparent redundancy between pcaA and cmaA2, another cyclopropane synthetase of M. tuberculosis thought to be involved in alpha-mycolate synthesis, we have disrupted the cmaA2 gene in virulent M. tuberculosis by specialized transduction. Inactivation of cmaA2 causes accumulation of unsaturated derivatives of both the methoxy- and ketomycolates. Analysis by proton NMR indicates that the mycolic acids of the cmaA2 mutant lack trans-cyclopropane rings but are otherwise intact with respect to cyclopropane and methyl branch content. Thus, cmaA2 is required for the synthesis of the trans cyclopropane rings of both the methoxymycolates and ketomycolates. These results define cmaA2 as a trans-cyclopropane synthetase and expand our knowledge of the substrate specificity of a large family of highly homologous mycolic acid methyl transferases recently shown to be critical to M. tuberculosis pathogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11092877&dopt=Abstract

Am J Nephrol. 2000 Sep-Oct;20(5):425-8.
Simultaneous occurrence of minimal change glomerular disease, sarcoidosis and Hashimoto's thyroiditis.

Nishimoto A, Tomiyoshi Y, Sakemi T, Kanegae F, Nakamura M, Ikeda Y, Shimazu K, Yonemitsu N.

Department of Internal Medicine, Saga Medical School, Saga, Japan.

We herein report a very rare case of a patient suffering from simultaneous occurrence of three immune disorders, i.e. Hashimoto's thyroiditis, sarcoidosis and minimal change glomerular disease. A 66-year-old man was admitted to our hospital for evaluation of nephrotic syndrome. Six months before admission, he was pointed out as having positive proteinuria, hypoalbuminemia and associated pretibial pitting edema. Initial laboratory data showed high gammaglobulinemia, high titers of both antimicrosomal and antithyroglobulin antibodies with normal thyroid function. Chest X-ray and CT scan revealed bilateral hilar lymphadenopathy with interstitial shadow. Ga-citrate scan disclosed positive accumulation in the thyroid glands, the mediastinum, the lungs and the kidneys. The diagnosis of minimal change nephritic syndrome and pulmonary sarcoidosis was made, based on the findings of transbronchial lung biopsy and kidney biopsy. After one and a half months of admission, thyroid function had gradually deteriorated. The histological findings of the thyroid were consistent with the features of Hashimoto's thyroiditis. Treatment with prednisolone and cyclophosphamide resulted in a decrease in urinary protein excretion, reduction in the size of mediastinal lymphadenopathy and disappearance of positive findings of Ga-citrate scan in the thyroid glands and the kidneys. Simultaneous occurrence of minimal change-glomerular disease, sarcoidosis and Hashimoto's thyroiditis in our case suggests that similar immunological abnormalities may be involved in the pathogenesis of the diseases. 2000 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11093004&dopt=Abstract

Eur J Immunol. 2000 Nov;30(11):3140-6.
Expression of MHC class II molecules contributes to lipopolysaccharide responsiveness.

Piani A, Hossle JP, Birchler T, Siegrist CA, Heumann D, Davies G, Loeliger S, Seger R, Lauener RP.

Division of Immunology, Hematology, Infectiology and Oncology, Zurich University Children's Hospital, Zurich, Switzerland.

Activation of phagocytes by lipopolysaccharide (LPS) causes synthesis and secretion of various mediators of inflammation. CD14, a glycosylphosphatidylinositol-anchored monocytic antigen serving as receptor for LPS, and members of the family of Toll-like receptors mediate cellular activation in response to LPS. Here we investigated whether expression of MHC class II molecules modified the response to LPS. Comparing LPS responsiveness of human and murine cells differing for expression of MHC class II molecules, we found that lack or a low level of expression of MHC class II molecules resulted in diminished secretion of pro-inflammatory cytokines following stimulation with LPS. Thus, expression of MHC class II molecules modifies LPS responsiveness, a finding suggesting that these molecules contribute to the pathogenesis not only of exotoxin-triggered toxic shock but also of endotoxin-triggered septic shock. Additionally to their role in antigen-specific immunity MHC class II molecules may influence the inflammatory response triggered by microbial constituents.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11093128&dopt=Abstract

Eur J Immunol. 2000 Nov;30(11):3181-9.
Induction of antibodies reactive to cardiac myosin and development of heart alterations in cruzipain-immunized mice and their offspring.

Giordanengo L, Maldonado C, Rivarola HW, Iosa D, Girones N, Fresno M, Gea S.

Inmunologia, Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Cordoba, Argentina.

Human and murine infection with Trypanosoma cruzi parasite is usually accompanied by strong humoral and cellular immune response to cruzipain, a parasite immunodominant antigen. In the present study we report that the immunization of mice with cruzipain devoid of enzymatic activity, was able to induce antibodies which bind to a 223-kDa antigen from a mouse heart extract. We identified this protein as the mouse cardiac myosin heavy chain by sequencing analysis. The study of IgG isotype profile revealed the occurrence of all IgG isotypes against cruzipain and myosin. IgG1 showed the strongest reactivity against cruzipain, whereas IgG2a was the main isotype against myosin. Anti-cruzipain antibodies purified by immunoabsorption recognized the cardiac myosin heavy chain, suggesting cross-reactive epitopes between cruzipain and myosin. Autoimmune response in mice immunized with cruzipain was associated to heart conduction disturbances. In addition, ultrastructural findings revealed severe alterations of cardiomyocytes and IgG deposit on heart tissue of immunized mice. We investigated whether antibodies induced by cruzipain transferred from immunized mothers to their offsprings could alter the heart function in the pups. All IgG isotypes against cruzipain derived from transplacental crossing were detected in pups' sera. Electrocardiographic studies performed in the offsprings born to immunized mothers revealed conduction abnormalities. These results provide strong evidence for a pathogenic role of autoimmune response induced by a purified T. cruzi antigen in the development of experimental Chagas' disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11093133&dopt=Abstract

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