The kynurenine pathway is important in cellular energy generation and limiting cellular ageing as it degrades about 90% of dietary tryptophan into the essential co-factor NAD+ (nicotinamide adenine dinucleotide). Prior to the production of NAD+, various intermediate compounds with neuroactivity (kynurenic acid, quinolinic acid) or antioxidant activity (3-hydroxykynurenine, picolinic acid) are synthesized. The kynurenine metabolites can participate in numerous neurodegenerative disorders (Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, and Parkinson disease) or other diseases such as AIDS, cancer, cardiovascular diseases, inflammation, and irritable bowel syndrome. Recently, the role of gut in affecting the emotional and cognitive centres of the brain has attracted a great deal of attention. In this review, we focus on the bidirectional communication between the gut and the brain, known as the gut-brain axis. The interaction of components of this axis, namely, the gut, its microbiota, and gut pathogens; tryptophan; the kynurenine pathway on tryptophan availability; the regulation of kynurenine metabolite concentration; and diversity and population of gut microbiota, has been considered.

No abstract

Advancement of science has gifted the human a longer life; however, as neuron cells do not regenerate, the number of people with neurodegeneration disorders rises with population aging. Neurodegeneration diseases occur as a result of neuronal cells loss caused by environmental factors, genetic mutations, proteopathies and other cellular dysfunctions. The negative direct or indirect contributions of various microorganisms in onset or severity of some neurodegeneration disorders and interaction between human immune system and pathogenic microorganisms has been portrayed in this review article. This association may explain the early onset of neurodegeneration disorders in some individuals, which can be traced through detailed study of health background of these individuals for infection with any microbial disease with neuropathogenic microorganisms (bacteria, fungi, viruses). A better understanding and recognition of the relation between microorganisms and neurodegeneration disorders may help researchers in development of novel remedies to avoid, postpone, or make neurodegeneration disorders less severe.

No abstract

Human gut microbiota contains a large, complex, dynamic microbial community of approximately 10 14 microbes from more than 1,000 microbial species, i.e., equivalent to 4 × 10 6 genes. Numerous evidence links gut microbiota with human health and diseases. Importantly, gut microbiota is involved in the development and function of the brain through a bidirectional pathway termed as the gut-brain axis. Interaction between gut microbiota and immune responses can modulate the development of neuroinflammation and cancer diseases in the brain. With respect of brain cancer, gut microbiota could modify the levels of antioxidants, amyloid protein and lipopolysaccharides, arginase 1, arginine, cytochrome C, granulocytemacrophage colony-stimulating factor signaling (GM-CSF), IL-4, IL-6, IL-13, IL-17A, interferon gamma (IFN-γ), reactive oxygen species (ROS), reactive nitrogen species (e.g., nitric oxide and peroxynitrite), short-chain fatty acids (SCFAs), tryptophan, and tumor necrosis factor-β (TGF-β). Through these modifications, gut microbiota can modulate apoptosis, the aryl hydrocarbon receptor (AhR), autophagy, caspases activation, DNA integrity, microglia dysbiosis, mitochondria permeability, T-cell proliferation and functions, the signal transducer and activator of transcription (STAT) pathways, and tumor cell proliferation and metastasis. The outcome of such interventions could be either oncolytic or oncogenic. This review scrutinizes the oncogenic and oncolytic effects of gut microbiota by classifying the modification mechanisms into (i) amino acid deprivation (arginine and tryptophan); (ii) kynurenine pathway; (iii) microglia dysbiosis; and (iv) myeloid-derived suppressor cells (MDSCs). By delineating the complexity of the gutmicrobiota-brain-cancer axis, this review aims to help the research on the development of novel therapeutic strategies that may aid the efficient eradication of brain cancers.

There are 17 human-biting ticks known in Australia. The bites of Ixodes holocyclus, Ornithodoros capensis, and Ornithodoros gurneyi can cause paralysis, inflammation, and severe local and systemic reactions in humans, respectively. Six ticks, including Amblyomma triguttatum, Bothriocroton hydrosauri, Haemaphysalis novaeguineae, Ixodes cornuatus, Ixodes holocyclus, and Ixodes tasmani may transmit Coxiella burnetii, Rickettsia australis, Rickettsia honei, or Rickettsia honei subsp. marmionii. These bacterial pathogens cause Q fever, Queensland tick typhus (QTT), Flinders Island spotted fever (FISF), and Australian spotted fever (ASF). It is also believed that babesiosis can be transmitted by ticks to humans in Australia. In addition, Argas robertsi, Haemaphysalis bancrofti, Haemaphysalis longicornis, Ixodes hirsti, Rhipicephalus australis, and Rhipicephalus sanguineus ticks may play active roles in transmission of other pathogens that already exist or could potentially be introduced into Australia. These pathogens include Anaplasma spp., Bartonella spp., Burkholderia spp., Francisella spp., Dera Ghazi Khan virus (DGKV), tick-borne encephalitis virus (TBEV), Lake Clarendon virus (LCV), Saumarez Reef virus (SREV), Upolu virus (UPOV), or Vinegar Hill virus (VINHV). It is important to regularly update clinicians' knowledge about tick-borne infections because these bacteria and arboviruses are pathogens of humans that may cause fatal illness. An increase in the incidence of tick-borne infections of human may be observed in the future due to changes in demography, climate change, and increase in travel and shipments and even migratory patterns of birds or other animals. Moreover, the geographical conditions of Australia are favorable for many exotic ticks, which may become endemic to Australia given an opportunity. There are some human pathogens, such as Rickettsia conorii and Rickettsia rickettsii that are not currently present in Australia, but can be transmitted by some human-biting ticks found in Australia, such as Rhipicephalus sanguineus, if they enter and establish in this country. Despite these threats, our knowledge of Australian ticks and tick-borne diseases is in its infancy.

No abstract

No abstract