Autonomic modification of intestinal smooth muscle contractility

Intestinal smooth muscle contracts rhythmically in the absence of nerve and hormonal stimulation because of the activity of pacemaker cells between and within the muscle layers. This means that the autonomic nervous system modifies rather than initiates intestinal contractions. The practical described here gives students an opportunity to observe this spontaneous activity and its modification by agents associated with parasympathetic and sympathetic nerve activity. A section of the rabbit small intestine is suspended in an organ bath, and the use of a pressure transducer and data-acquisition software allows the measurement of tension generated by the smooth muscle of intestinal walls. The application of the parasympathetic neurotransmitter ACh at varying concentrations allows students to observe an increase in intestinal smooth muscle tone with increasing concentrations of this muscarinic receptor agonist. Construction of a concentration-effect curve allows students to calculate an EC50 value for ACh and consider some basic concepts surrounding receptor occupancy and activation. Application of the hormone epinephrine to the precontracted intestine allows students to observe the inhibitory effects associated with sympathetic nerve activation. Introduction of the drug atropine to the preparation before a maximal concentration of ACh is applied allows students to observe the inhibitory effect of a competitive antagonist on the physiological response to a receptor agonist. The final experiment involves the observation of the depolarizing effect of K+ on smooth muscle. Students are also invited to consider why the drugs atropine, codeine, loperamide, and botulinum toxin have medicinal uses in the management of gastrointestinal problems.

Metabolism of mineral-sorbed organic matter depends upon microbial lifestyle in fluvial ecosystems

In fluvial ecosystems mineral erosion, carbon (C) and nitrogen (N) fluxes are linked via organo-mineral complexation, where dissolved organic molecules bind to mineral surfaces. Biofilms and suspended aggregates represent major aquatic microbial lifestyles whose relative importance changes predictably through fluvial networks. We tested how organo-mineral sorption affects aquatic microbial metabolism, using organo-mineral particles containing a mix of ¹³C, ¹⁵N-labelled amino acids. We traced ¹³C and ¹⁵N retention within biofilm and suspended aggregate biomass and its mineralisation. Organo-mineral complexation restricted C and N retention within biofilms and aggregates and also their mineralisation. This reduced the efficiency with which biofilms mineralise C and N by 30 % and 6 %. By contrast, organo-minerals reduced the C and N mineralisation efficiency of suspended aggregates by 41 % and 93 %. Our findings show how organo-mineral complexation affects microbial C:N stoichiometry, potentially altering the biogeochemical fate of C and N within fluvial ecosystems.

Lipopolysaccharide modification in Gram-negative bacteria during chronic infection

The Gram-negative bacterial lipopolysaccharide (LPS) is a major component of the outer membrane that plays a key role in host-pathogen interactions with the innate immune system. During infection, bacteria are exposed to a host environment that is typically dominated by inflammatory cells and soluble factors, including antibiotics, which provide cues about regulation of gene expression. Bacterial adaptive changes including modulation of LPS synthesis and structure are a conserved theme in infections, irrespective of the type or bacteria or the site of infection. In general, these changes result in immune system evasion, persisting inflammation, and increased antimicrobial resistance. Here, we review the modifications of LPS structure and biosynthetic pathways that occur upon adaptation of model opportunistic pathogens (Pseudomonas aeruginosa, Burkholderia cepacia complex bacteria, Helicobacter pylori and Salmonella enterica) to chronic infection in respiratory and gastrointestinal sites. We also discuss the molecular mechanisms of these variations and their role in the host-pathogen interaction.