The ingestion of fatty meals is associated with a transient, low-grade systemic inflammatory response in human subjects, involving the activation of circulating monocytes and the secretion of pro-inflammatory cytokines. However, it is not yet clear how different foodstuffs may promote inflammatory signalling. In a screen of forty filter-sterilised soluble extracts from common foodstuffs, seven were found to induce the secretion of TNF-α and IL-6 from human monocytes in vitro. To investigate what may differentiate inflammatory from non-inflammatory food extracts, stimulants of Toll-like receptor (TLR) 2 and TLR4 were quantified using human embryonic kidney-293 cells transfected with each TLR, and calibrated with defined bacterial lipopeptide (BLP) and lipopolysaccharide (LPS) standards. These assays revealed that while most foods contained undetectable levels of TLR2 or TLR4 stimulants, all TNF-α-inducing foods contained stimulants of either TLR2 (up to 1100 ng BLP-equivalent/g) or TLR4 (up to 2700 ng LPS-equivalent/g) in both the soluble and insoluble fractions. TLR stimulants were present mainly in meat products and processed foods, but were minimal or undetectable in fresh fruit and vegetables. The capacity of food extracts to induce TNF-α secretion in monocytes correlated with the content of both TLR2 (r 0·837) and TLR4 stimulants (r 0·748), and was completely abolished by specific inhibition of TLR2 and TLR4. LPS and BLP were found to be highly resistant to typical cooking times and temperatures, low pH and protease treatment. In conclusion, apparently unspoiled foodstuffs can contain large quantities of stimulants of TLR2 and TLR4, both of which may regulate their capacity to stimulate inflammatory signalling.

The involvement of endotoxins in Trypanosoma brucei brucei infection in CD-1 mice was investigated by the Limulus amoebocyte lysate (LAL) test. At 7 days post-infection mean serum endotoxin level was elevated by 2·5 times (36·4 pg/ml cf. control 14·25 pg/ml, P < 0·001) and a similar increase was maintained throughout the infection (survival 28–35 days). Purified disrupted parasites contained significant endotoxin activity (mean value 280 pg/mg protein). The mouse infections were also associated with progressive Gram-negative bacteraemia (present in 4 Out of 5 infected animals by day 28 p.i.). The increased endotoxin levels may be due to parasite products, the products of intercurrent bacterial infections, other unidentified sources (e.g. from the gut), or a combination of these. It is concluded that the raised endotoxins may be important contributive factors in the pathogenesis of experimental murine trypanosomiasis.

Crystals of a local isolate of Bacillus thuringiensis variety israelensis were isolated by centrifugation on a continuous sucrose gradient (40–70%). Analysis of the crystals by SDS-PAGE revealed three major protein subunits of Mr˜25,000, ˜66,000 and Mr˜140,000. The crystals were solubilised using high pH and reducing conditions. Analysis of the soluble (protoxin) and insoluble fractions by SDS-PAGE showed the presence of proteins of Mr˜21,000 and ˜61,000, respectively. Proteolytic treatment of these fractions resulted in no apparent change in the molecular weights of the proteins. The crystals contained carbohydrate moieties as determined by periodic acid Schiff (PAS) and fluorescein isothiocyanate (FITC) Concanavalin A staining. In double radial immunodiffusion experiments, antisera raised against the Mr˜21,000 and ˜66,000 subunits did not react with other B. thuringiensis protoxins known to be active against the tsetse fly, Glossina morsitans morsitans, and the stemborer, Chile partellus.

This study presents animal experiments on endotoxin (lipopolysaccharides: LPS) damage to the inner ear with special reference to the stria vascularis. The experimental group animals (albino guinea pigs) were injected with LPS into the perilymphatic space. Pyrogen-free saline (PFS) was injected into the control group. Strial structural evaluation and hearing tests were carried out before and one, three and five days after treatment. In PFS-treated (control) ears, no significant change was found either in hearing or structure. However, thresholds of Nl/Pl were elevated and latencies prolonged in LPS-treated ears. They had severe strial damage mainly to the cellular organelles. The mitochondria became swollen with a disordered, broken, degenerated or absent crest. Secondary lysosomes and autophagosomes increased in number with the presence of medulative inclusions. Na+-K+-ATPase reactant was obviously diminished. It is concluded that LPS-induced strial ototoxicityproduces ion imbalance, causing changesin endolymph composition and energy failure in the organ of Corti and is also responsible for the pathogenesis of inner ear sequelae secondary to otitis media.