PubMed HealthSearch

PubMed · 335089

Antibody-coated bacteria in the ejaculate: a possible test for prostatitis.

Abstract

An immunofluorescence technique was used to study antibody coating of bacteria in ejaculates from 14 healthy individuals and 51 patients with complaints compatible with the diagnosis of prostatitis. Quantitative bacteriological cultures in the ejaculate were positive in 2 healthy individuals (14%) and in 25 patients with prostatic symptoms (49%). Antibody-coated bacteria could be demonstrated in 25 patients with prostatic symptoms (49%), 8 of whom had negative bacterial cultures, but in none of the healthy individuals. All 5 patients with epididymitis had antibody-caoted bacteria in the ejaculate. The 13 patients with antibody-coated bacteria in the ejaculate were given antibiotic treatment and the bacteria disappeared in 8 cases. The results document the presence of a (presumably local) immune response in bacterial prostatitis. Antibody coating of bacteria in the ejaculate seems to be helpful in the diagnosis of bacterial prostatitis.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Riedasch, E Ritz, K Möhring, U Ikinger. 1977. Antibody-coated bacteria in the ejaculate: a possible test for prostatitis.. https://doi.org/10.1016/s0022-5347(17)58193-8

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

ERBB3 overexpression due to miR-205 inactivation confers sensitivity to FGF, metabolic activation, and liability to ERBB3 targeting in glioblastoma.

In glioblastoma (GBM), the most frequent and lethal brain tumor, therapies suppressing recurrently altered signaling pathways failed to extend survival. However, in patient subsets, specific genetic lesions can confer sensitivity to targeted agents. By exploiting an integrated model based on patient-derived stem-like cells, faithfully recapitulating the original GBMs in vitro and in vivo, here, we identify a human GBM subset (∼9% of all GBMs) characterized by ERBB3 overexpression and nuclear accumulation. ERBB3 overexpression is driven by inheritable promoter methylation or post-transcriptional silencing of the oncosuppressor miR-205 and sustains the malignant phenotype. Overexpressed ERBB3 behaves as a specific signaling platform for fibroblast growth factor receptor (FGFR), driving PI3K/AKT/mTOR pathway hyperactivation, and overall metabolic upregulation. As a result, ERBB3 inhibition by specific antibodies is lethal for GBM stem-like cells and xenotransplants. These findings highlight a subset of patients eligible for ERBB3-targeted therapy.

Antibodies

Inhibition of collagen-induced platelet aggregation by antibodies to distinct types of collagens.

Aggregation of platelets by fibrils formed from collagens type I, II and III could be inhibited by coating the fibrils with anti-collagen antibodies or Fab fragments. Similar results were obtained in a clot-retraction assay. Inhibition was achieved with stoichiometric amounts of antibodies and was specific for each type of collagen. Aggregation caused by a mixture of type-I and -III collagens could only be inhibited by a mixture of antibodies against both collagens. The data show that each interstitial collagen is capable of interacting with platelets and do not support the concept of an outstanding activity of type-III collagen.

Antibodies