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Infect Immun. 2003 Jun;71(6):3619-22.
The FimH A27V mutation is pathoadaptive for urovirulence in Escherichia coli B2 phylogenetic group isolates.

Hommais F, Gouriou S, Amorin C, Bui H, Rahimy MC, Picard B, Denamur E.

INSERM U458, Hopital Robert Debre Centre d'Etude du Polymorphisme Humain, Hopital Saint Louis, Paris, France.

Correlations between FimH mutations and virulence were established by studying a collection of human commensal and extraintestinal pathogenic Escherichia coli natural isolates. Pathoadaptive (A27V and, to a lesser extent, A119V) and "commensal-adaptive" (A202V) mutations were evidenced in B2 phylogenetic group strains. fimH phylogenetic analysis indicates that these pathoadaptive mutations occurred several times.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12761149&dopt=Abstract

J Biol Chem. 2003 Jul 25;278(30):27721-8. Epub 2003 May 20.
ERK 1/2- and JNKs-dependent synthesis of interleukins 6 and 8 by fibroblast-like synoviocytes stimulated with protein I/II, a modulin from oral streptococci, requires focal adhesion kinase.

Neff L, Zeisel M, Druet V, Takeda K, Klein JP, Sibilia J, Wachsmann D.

Laboratoire d'Immunologie et de Biochimie Bacterienne, Inserm U392, Universite Louis Pasteur de Strasbourg, France.

Protein I/II, a pathogen-associated molecular pattern from oral streptococci, is a potent inducer of interleukin-6 (IL-6) and IL-8 synthesis and release from fibroblast-like synoviocytes (FLSs), cells that are critically involved in joint inflammation. This synthesis implicates ERK 1/2 and JNKs as well as AP-1-binding activity and nuclear translocation of NF-kappaB. The mechanisms by which protein I/II activates MAPKs remain, however, elusive. Because focal adhesion kinase (FAK) was proposed to play a role in signaling to MAPKs, we examined its ability to contribute to the MAPKs-dependent synthesis of IL-6 and IL-8 in response to protein I/II. We used FAK-/- fibroblasts as well as FAK+/+ fibroblasts and FLSs transfected with FRNK, a dominant negative form of FAK. The results demonstrate that IL-6 and IL-8 release in response to protein I/II was strongly inhibited in both protein I/II-stimulated FAK-/- and FRNK-transfected cells. Cytochalasin D, which inhibits protein I/II-induced phosphorylation of FAK (Tyr-397), had no effect either on activation of ERK 1/2 and JNKs or on IL-6 and IL-8 release. Taken together, these results indicate that IL-6 and IL-8 release by protein I/II-activated FLSs is regulated by FAK independently of Tyr-397 phosphorylation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12761229&dopt=Abstract

J Am Soc Nephrol. 2003 Jun;14(6):1519-22.
A gene locus for steroid-resistant nephrotic syndrome with deafness maps to chromosome 14q24.2.

Ruf RG, Wolf MT, Hennies HC, Lucke B, Zinn C, Varnholt V, Lichtenberger A, Pasch A, Imm A, Briese S, Lennert T, Fuchshuber A, Nurnberg P, Hildebrandt F.

Department of Pediatrics, University of Michigan, Ann Arbor, 48109, USA.

Steroid-resistant nephrotic syndrome (SRNS) leads to end-stage renal disease (ESRD) in childhood or young adulthood. Positional cloning for genes causing SRNS has opened the first insights into the understanding of its pathogenesis. This study reports a genome-wide search for linkage in a consanguineous Palestinian kindred with SRNS and deafness and detection of a region of homozygosity on chromosome 14q24.2. Multipoint analysis of 12 markers used for further fine mapping resulted in a LOD score Z(max) of 4.12 (theta = 0) for marker D14S1025 and a two-point LOD score of Z(max) = 3.46 (theta = 0) for marker D14S77. Lack of homozygosity defined D14S1065 and D14S273 as flanking markers to a 10.7 cM interval. The identification of the responsible gene will provide new insights into the molecular basis of nephrotic syndrome and sensorineural deafness.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12761252&dopt=Abstract

Pediatr Res. 2003 Sep;54(3):297-305. Epub 2003 May 21.
Burkholderia cepacia-induced IL-8 gene expression in an alveolar epithelial cell line: signaling through CD14 and mitogen-activated protein kinase.

Reddi K, Phagoo SB, Anderson KD, Warburton D.

Developmental Biology Program, Childrens Hospital, Los Angeles Research Institute, 4650 Sunset Boulevard, Los Angeles, CA 90027, USA.

Burkholderia cepacia is a prevalent pulmonary pathogen in patients with cystic fibrosis (CF). The lung pathology observed in patients with CF is postulated to be due to an overexpression of chemokines. This study investigated the induction of the neutrophil chemoattractant chemokine IL-8 and the signaling pathways activated by B. cepacia-infected human lung epithelial A549 (HLE) cells. Cells were infected with B. cepacia (genomovar III of the B. cepacia complex), and reverse transcriptase-PCR and ELISA for the cytokines were performed. B. cepacia (multiplicity of infection > or =4:1) induced HLE cells to significantly secrete IL-8 in a more potent manner than the predominant CF pathogen Pseudomonas aeruginosa (multiplicity of infection > or =64:1). IL-8 secretion by B. cepacia-infected HLE cells was abrogated by the gene transcription inhibitor actinomycin D and the protein translation inhibitor cycloheximide, confirming that B. cepacia-induced IL-8 secretion was mediated through de novo protein synthesis. Treatment of B. cepacia with proteinase K failed to down-regulate IL-8 secretion; furthermore, IL-8 secretion by B. cepacia-infected HLE cells was abrogated by > or =80% in the presence of anti-CD14 [specific lipopolysaccharide (LPS) receptor] antibody, thus suggesting that the IL-8-inducing component of B. cepacia was LPS and therefore dependent on CD14. The p38 mitogen-activated protein kinase (MAPK) inhibitor and the extracellular signal-regulated kinase MAPK inhibitor significantly abrogated IL-8 secretion by B. cepacia-infected HLE cells (SB203580, > or =80% inhibition; PD98059, > or =30% inhibition). In conclusion, B. cepacia-induced IL-8 secretion in A549 airway epithelial cells is more potent than P. aeruginosa; is mediated through LPS, which is CD14 dependent; and involves activation of the p38 and ERK MAPK pathways.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12761358&dopt=Abstract [PubMed - in process]

Korean J Ophthalmol. 1998 Dec;12(2):103-7.
The ultrastructure of corneal epithelium after co-cultivation with herpes simplex virus.

Lee DY, Ko MK, Choe JK.

Department of Ophthalmology, School of Medicine, Hanyang University, Seoul, Korea.

To elucidate the ultrastructural change of corneal epithelium co-cultured with herpes simplex virus (HSV), the corneal epithelium of 3 rabbits was excised and cultivated in culture media. After 7 days, the Kos strain of herpes simplex virus was inoculated in the cultured cornea epithelium until cytopathic effect was occurred. It was fixed in the solution of 3% glutaraldehyde and examined with electronmicroscope. In co-cultured cells, the intercellular spaces had increased and microvilli were seen prominently. The virus particles that initiated the infection by fusing the viral envelope with the plasma membrane were also seen. The nuclear degeneration in an infected cell was prominent. The nuclear membrane was folded markedly, and the chromatin was degraded, condensed and displaced toward the nuclear membrane. Numerous viral particles and inclusion bodies were present in the nuclei. These findings suggest that the infectious process of herpes simplex virus in the human corneal epithelium may occur in a similar way. This result would be helpful in understanding the pathogenesis of herpes simplex epithelial keratitis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10188370&dopt=Abstract

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