Silicon fertilisation affects morphological and immune defences of an insect pest and enhances plant compensatory growth

Herbivorous insects have evolved various anti-predator defences, including morphological, behavioural, and immune defences, which can make biocontrol of herbivorous pests challenging. Silicon (Si) accumulation in plants is a potent physical defence against mandibulate insects. However, it remains uncertain how Si affects the anti-predator defences of insect herbivores and plant defences following herbivory. We grew the model grass, Brachypodium distachyon, hydroponically with (+Si) or without (–Si) Si and investigated the plant-mediated effects of Si on the anti-predator defences of the cotton bollworm, Helicoverpa armigera, integrating morphological (i.e. integument resistance and thickness), behavioural, and immune defences. We also examined the effects of Si on plant compensatory growth and leaf trichome production. Larval growth, leaf consumption, and integument resistance were lower when feeding on +Si plants compared to when feeding on –Si plants. Larval integument thickness, defensive behaviours, haemocyte density, and lysozyme-like activity in the haemolymph were unaffected by Si. Larvae fed on +Si plants had higher haemolymph phenoloxidase (PO) and total-PO activities than larvae fed on –Si plants, although this did not enhance the melanisation response of larvae. Furthermore, Si supplies increased plant compensation for herbivory and constitutive trichome production, whereas herbivory induced trichome production only on –Si plants. We provide the first evidence for plant-mediated effects of Si on anti-predator defences of an insect herbivore. We suggest that the lower integument resistance of larvae when feeding on Si-supplemented plants could contribute to their vulnerability to natural enemies and that high PO activity may impose fitness costs (e.g. delayed development).

Between the Devil and the Deep Blue Sea: Non-Coding RNAs Associated with Transmissible Cancers in Tasmanian Devil, Domestic Dog and Bivalves

Currently there are nine known examples of transmissible cancers in nature. They have been observed in domestic dog, Tasmanian devil, and six bivalve species. These tumours can overcome host immune defences and spread to other members of the same species. Non-coding RNAs (ncRNAs) are known to play roles in tumorigenesis and immune system evasion. Despite their potential importance in transmissible cancers, there have been no studies on ncRNA function in this context to date. Here, we present possible applications of the CRISPR/Cas system to study the RNA biology of transmissible cancers. Specifically, we explore how ncRNAs may play a role in the immortality and immune evasion ability of these tumours.

Dissecting Host-Pathogen Interactions in TB Using Systems-Based Omic Approaches

Tuberculosis (TB) is a devastating infectious disease that kills over a million people every year. There is an increasing burden of multi drug resistance (MDR) and extensively drug resistance (XDR) TB. New and improved therapies are urgently needed to overcome the limitations of current treatment. The causative agent, Mycobacterium tuberculosis (Mtb) is one of the most successful pathogens that can manipulate host cell environment for adaptation, evading immune defences, virulence, and pathogenesis of TB infection. Host-pathogen interaction is important to establish infection and it involves a complex set of processes. Metabolic cross talk between the host and pathogen is a facet of TB infection and has been an important topic of research where there is growing interest in developing therapies and drugs that target these interactions and metabolism of the pathogen in the host. Mtb scavenges multiple nutrient sources from the host and has adapted its metabolism to survive in the intracellular niche. Advancements in systems-based omic technologies have been successful to unravel host-pathogen interactions in TB. In this review we discuss the application and usefulness of omics in TB research that provides promising interventions for developing anti-TB therapies.

Constitutive TRIM22 Expression in the Respiratory Tract Confers a Pre-Existing Defence Against Influenza A Virus Infection

The induction of antiviral effector proteins as part of a homeostatically controlled innate immune response to infection plays a critical role in limiting the propagation and transmission of respiratory pathogens. However, the prolonged induction of this immune response can lead to lung hyperinflammation, tissue damage, and respiratory failure. We hypothesized that tissues exposed to the constant threat of infection may constitutively express higher levels of antiviral effector proteins to reduce the need to activate potentially harmful innate immune defences. By analysing transcriptomic data derived from a range of human tissues, we identify lung tissue to express constitutively higher levels of antiviral effector genes relative to that of other mucosal and non-mucosal tissues. By using primary cell lines and the airways of rhesus macaques, we show the interferon-stimulated antiviral effector protein TRIM22 (TRIpartite Motif 22) to be constitutively expressed in the lung independently of viral infection or innate immune stimulation. These findings contrast with previous reports that have shown TRIM22 expression in laboratory-adapted cell lines to require interferon stimulation. We demonstrate that constitutive levels of TRIM22 are sufficient to inhibit the onset of human and avian influenza A virus (IAV) infection by restricting the onset of viral transcription independently of interferon-mediated innate immune defences. Thus, we identify TRIM22 to confer a pre-existing (intrinsic) intracellular defence against IAV infection in cells derived from the respiratory tract. Our data highlight the importance of tissue-specific and cell-type dependent patterns of pre-existing immune gene expression in the intracellular restriction of IAV from the outset of infection.

Silicon Fertilisation Affects Morphological and Immune Defences of an Insect Pest and Enhances Plant Compensatory Growth

Insect herbivores employ various defences, including morphological, behavioural, and immune responses against their natural enemies (e.g., predators, parasitoids) which can make biocontrol of herbivorous pests challenging. Silicon (Si) accumulation in plants is a potent physical defence against herbivores. However, it remains uncertain how Si affects pest defences to their enemies and plant defences following herbivore attack. We grew the model grass, Brachypodium distachyon, hydroponically with (+Si) or without (–Si) Si and investigated the impacts of Si on morphological (integument resistance and thickness), behavioural (flee, headrear, thrash, and regurgitation), and immune defences of the cotton bollworm, Helicoverpa armigera. We further examined the effects of Si on plant compensatory growth and leaf trichome production. Larval growth, leaf consumption, and integument resistance were lower when feeding on +Si plants compared to when feeding on –Si plants. Larval integument thickness, defensive behaviours, hemocyte density and lysozyme-like activity in the hemolymph were unaffected by Si. Larvae fed on +Si plants had higher hemolymph phenoloxidase (PO) and total-PO activities than larvae fed on –Si plants, although this did not enhance larval melanisation response. Furthermore, Si supply increased plant compensatory growth and constitutive trichome production whereas herbivory induced trichome production only on –Si plants. We provide the first evidence that Si fertilisation affects insect defences in addition to reducing their growth and feeding. Lower integument resistance might enhance larval vulnerability to parasitoids and pathogens and higher PO activities could impose fitness costs (e.g., delayed development), potentially increasing overall insect susceptibility to enemies.

Case report of COVID-19 positive new born with necrotizing enterocolitis (NEC)

COVID-19 caused by SARS-Cov-2 virus has spread rapidly across the world. Children are just as like as adult to become infected with virus but have lesser symptoms and less severity of the disease. Necrotizing enterocolitis is one of the common gastrointestinal emergencies in neonatal intensive care unit. More than 85% of cases of NEC occur among preterm and very low birth weight. Preterm babies are vulnerable to develop NEC because of high incidence of perinatal distress factor, stasis of gut due to autonomic immaturity, poor barrier function of gut or immune defences, lack of feeding with human milk and higher incidence of nosocomial infections. During the current COVID-19 pandemic, no similar finding has been reported in the neonatal population to date. In this review we summarize the case report of two newborns admitted in our NICU who were COVID 19 positive presented to us with symptoms suggestive of necrotizing enterocolitis (NEC) and their outcome based on presence of comorbidity. Our case reports two case of two COVID-19 positive newborns admitted in our NICU with history, examination and investigations suggestive of necrotizing enterocolitis. Early initiation of antibiotics covering bowel flora, bowel rest and resuscitation, similar to our tried and true medical management of NEC, should be considered for initial management to avoid surgical intervention

Community-Acquired Methicillin-Resistant Staphylococcus Aureus an Important Enemy against us; Why Investigation of Their Main Toxins Reveals Contradictory Data

Community-Acquired Methicillin-resistant Staphylococcus aureus (CA-MRSA) strains are serious human pathogens because of their micro floral abilities; resistance to clinically important antibiotics and ability to evade the host immune defences. Panton–Valentine leucocidin (PVL) and Phenol-soluble modulins (PSMs) are the main important virulence factors of CA-MRSA. The aim of this work was to provide an explanation on why there are contradictory findings in studies of PVL and PSMs. Several factors such as differences in growth media or in injection mode, species-specific interaction, contamination in culture supernatants, the concentration of toxin, and exposure time that have an effect on conducting of these studies were discussed in this paper.

The natural history of defences

Hosts can avoid infections by behavioural changes and by body walls. After infection, hosts can change their behaviours to reduce the effects of parasitism. Immune defences have different arms (humoral or cellular), and organization (innate, adaptive). Innate immunity consists of a collection of different systems that are evolutionarily very old. Adaptive immunity, based on expansion of specific lymphocytes, evolved in the higher vertebrates. Immune defences are regulated tightly and based on receptors that can recognize parasites (or their activity). This triggers a complex signalling cascade that results in the production of further signalling compounds and effectors. Important protein families, e.g. the immunoglobulins, form the molecular backbone. A key to efficient defences is the diversification of receptors, such as the highly evolved somatic diversification processes of advanced adaptive immunity. The microbiota adds to defences in many ways. Immune memory and priming occur throughout the tree of life.

Specificity

infect a number of host species. This host range is given by an ecological filter (the possibility of encounter) and a physiological one (the capacity of establishing an infection). Host ranges typically are right-skewed, with most parasites infecting only a few, but few infecting very many hosts. There is no universally valid hypothesis that explains host range. However, a number of factors contribute to host range, such as geographical range, phylogenetic distance, host predictability, and parasite virulence. Specificity and cross-reactivity of immune defences are important mechanisms. Moreover, immune memory is based on specificity; transgenerational immune priming protects offspring when parents have already been exposed to the same or similar parasites.

Ecological immunology

Infections and parasite loads vary among hosts. Variation results from ecological, genetic, and immunological factors. Immune defences provide benefits as well as costs and are, therefore, a compromise. Costs result from trade-offs with other needs and can be genetically encoded or plastic (i.e. can change depending on circumstances). Costs are physiological (e.g. energy consumption) or based on evolved genetic covariance. Self-damage (immunopathology) is a further, important cost. Natural selection should optimize the costs and benefits of defences and thus leads to various outcomes in terms of specificity, response delay and strength, or the formation of memory. Moreover, hosts can either resist an infection by eventual clearance, or tolerate the consequences of parasitism.