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In 1910, Dr Crippen, an American homoeopathic physician living in London, attempted to dispose of the remains of his wife, Cora, by dissolving her torso in a bath of acid. [...]

Gut bacteria stimulate signaling pathways that promote tolerance to infection and limit physiological damage.

The subcutaneous fat layer thickens during infection and stimulates adipocytes to secrete a protective peptide.

Benthic marine larval development is triggered by a bacterially expressed structure of phage origin.

The abundant marine cyanobacterium Prochlorococcussheds membrane vesicles that may contribute to carbon budgets.

Soluble lymphotoxin plays a paracrine role in controlling immunoglobulin A responses and regulating gut microbiota.

Enzymes secreted by a bacterial pathogen turn immune responses against themselves.

The heart drug digoxin can be inactivated by a strain of gut microbe bearing a cardiac glycoside reductase operon.

A surface protein of Plasmodium falciparumookinetes allows it to evade the complement-like responses of Anopheles gambiae.

Interaction of a platelet protein and a red cell protein enables platelets to attack malarial parasites inside red cells.

Cooperating groups of bacteria resist infiltration by noncooperating cheats by co-regulating shared and individual products.

Expression of nitric oxide synthase followed by peroxidase activity makes Plasmodiumvisible to the insect’s complement system.

Sulfide formation helps to protect various bacteria from antibiotic toxicity.

During growth arrest, bacteria tolerate the presence of antibiotics thanks to mechanisms that protect against oxidant stress.

Successful development of fruit flies depends on a gut bacterium that interacts with its host’s insulin-signaling pathway.

A beetle species synthesizes an antimicrobial peptide to constrain a bacterial symbiont in specialized organs.

Polymorphic receptors prevent cheaters from avoiding altruistic cell death in Dictyostelium.

An RNA virus of a parasite binds to human Toll-like receptor 3 and modulates host immune responses to the parasite.

Scientists and policy-makers must help to achieve a public consensus about the value of vaccination to individuals and society.

The genome of a third mosquito species reveals distinctions related to vector capacities and habitat preferences.

Early immune priming limits malaria parasite infection of mosquitoes.

A microfluidics device reveals a common response of bacterial plankton to sulfur compounds emitted by marine algae.

Variable maturation of a dengue viral antigen results in incomplete neutralization and promotes secondary pathology.

A specific virus encodes membrane components that broadcast cell death and population demise of its coccolithophore host.

Bacteria deploy nitric oxide synthases to counter oxidative stress from natural toxins and antibiotic drugs.

A family of molecules, apparently unique to mosquitoes, binds to invading parasites and initiates innate immune responses.

A family of proteins is identified that binds to foreign cytoplasmic DNA in mammalian cells and regulates the immune response.

In addition to an antiseptic function, phenazines—pigmented antibiotics made by bacteria—organize colony structure by activating a superoxidative stress regulator.

Many bacterial pathogens sense that they are in a potential host because they can detect adrenergic molecules. These organisms share a sensor kinase that picks up the signal and relays it to virulence gene loci, thus kicking in the responses needed to ensure bacterial establishment. This pathway makes a good target for broad-spectrum antibiotic development because virulence inhibition should not present a strong selective pressure for resistance. Rasko et al. have had some success with this approach using a nontoxic small-molecule inhibitor of the sensor kinase QseC, which blocks signaling in a sensitive and specific manner. In animal models, the inhibitor was somewhat effective against gastrointestinal infections with enterohemorrhagic E. coliand Salmonella typhimurium. Encouragingly, the lead molecule was more effective against the systemic pathogen Francisella tularensis: A single oral dose protected 80% of infected mice from death.D. A. Rasko, C. G. Moreira, D. R. Li, N. C. Reading, J. M. Ritchie, M. K. Waldor, N. Williams, R. Taussig, S. Wei, M. Roth, D. T. Hughes, J. F. Huntley, M. W. Fina, J. R. Falck, V. Sperandio, Targeting QseC signaling and virulence for antibiotic development. Science321, 1078-1080 (2008). [Abstract][Full Text]

Cells of the pathogenic bacterium Proteus mirabilisclump together to form colonies that, on meeting other colonies, can distinguish self from foreigners. Proteusdetects, then deters, interlopers of the same species using polypeptide weapons called proticines. Gibbs et al.investigated the genetic basis of this self-non-self recognition system in Proteusand discovered a locus of six genes that seem to constitute general and specific recognition determinants, as well as accessory genes. Within infected hosts, P. mirabilisinfections are usually clonal, so this recognition system could be a way for an established clone to prevent superinfection by another clone and to avoid competition. K. A. Gibbs, M. L. Urbanowski, E. P. Greenberg, Genetic determinants of self identity and social recognition in bacteria. Science321, 256-259 (2008). [Abstract][Full Text]

Many natural signals progress in a readily predictable sequence. For instance, after being eaten, a bacterium will perceive a sudden temperature rise followed by a drop in oxygen levels. Tagkopoulos et al. (see the Perspective by Baliga) investigated Escherichia coli’spredictive powersin a combination of in silicoand chemostat experiments. On exposure to a large temperature change, E. colican shift from aerobiosis to anaerobiosis even in the presence of 18% oxygen. This might seem maladaptive, but it means that the organism will have a competitive edge as soon as it encounters the zoo of microorganisms in the oxygen-starved lower gut. Furthermore, the authors were able to "train" the organisms to adapt metabolically to "unnatural" sequences of events, e.g., elevated temperature followed by high oxygen. I. Tagkopoulos, Y.-C. Liu, S. Tavazoie, Predictive behavior within microbial genetic networks. Science320, 1313-1317 (2008). [Abstract][Full Text]N. S. Baliga, The scale of prediction. Science320, 1297-1298 (2008). [Summary][Full Text]

M proteins are antigenically variable cell-surface virulence factors of group A Streptococcus(GAS). This organism is an important cause of human illness and notably provokes the autoimmune disease rheumatic fever. McNamara et al.examined a fragment of M1 that binds to host fibrinogen and promotes inflammation. The M1 protein consists of α-helical coiled coils bearing distinctive structural features that impart irregularity and instability to the coiled coil. These features mimic muscle myosin and tropomyosin, which may explain postinfection autoimmune responses. Mice immunized with a mutant, stabilized M protein exhibited reduced harmful inflammation without compromising protective immune responses.C. McNamara, A. S. Zinkernagel, P. Macheboeuf, M. W. Cunningham, V. Nizet, P. Ghosh, Coiled-coil irregularities and instabilities in group A StreptococcusM1 are required for virulence. Science319, 1405-1408 (2008). [Abstract][Full Text]