scholarly journals Glyphosate Inhibits Melanization and Increases Insect Susceptibility to Infection

2020 ◽  
Author(s):  
Daniel F. Q. Smith ◽  
Emma Camacho ◽  
Raviraj Thakur ◽  
Alexander J. Barron ◽  
Nichole A. Broderick ◽  
...  

SUMMARYMelanin is a black-brown pigment found throughout all kingdoms of life playing diverse roles including: UV protection, thermoregulation, oxidant scavenging, arthropod immunity, and microbial virulence. Given melanin’s broad functions in the biosphere, particularly in insect immune defenses, it is important to understand how environmental conditions affect melanization. Glyphosate, the most widely used herbicide, inhibits melanin production. Here we elucidate the mechanism underlying glyphosate’s inhibition of melanization demonstrate the herbicide’s multifactorial effects on insects. Glyphosate acts as an antioxidant and disrupts the oxidation-reduction balance of melanization. The drug reduced wax moth larvae survival after infection, increased parasite burden in malaria-transmitting mosquitoes, and altered midgut microbiome composition in adult mosquitoes. These findings suggest that glyphosate’s environmental accumulation could contribute to the so called insect apocalypse, characterized by species declines, by rendering them more susceptible to microbial pathogens due to melanization inhibition, immune impairment, and perturbations in microbiota composition.

PLoS Biology ◽  
2021 ◽  
Vol 19 (5) ◽  
pp. e3001182
Author(s):  
Daniel F. Q. Smith ◽  
Emma Camacho ◽  
Raviraj Thakur ◽  
Alexander J. Barron ◽  
Yuemei Dong ◽  
...  

Melanin, a black-brown pigment found throughout all kingdoms of life, has diverse biological functions including UV protection, thermoregulation, oxidant scavenging, arthropod immunity, and microbial virulence. Given melanin’s broad roles in the biosphere, particularly in insect immune defenses, it is important to understand how exposure to ubiquitous environmental contaminants affects melanization. Glyphosate—the most widely used herbicide globally—inhibits melanin production, which could have wide-ranging implications in the health of many organisms, including insects. Here, we demonstrate that glyphosate has deleterious effects on insect health in 2 evolutionary distant species, Galleria mellonella (Lepidoptera: Pyralidae) and Anopheles gambiae (Diptera: Culicidae), suggesting a broad effect in insects. Glyphosate reduced survival of G. mellonella caterpillars following infection with the fungus Cryptococcus neoformans and decreased the size of melanized nodules formed in hemolymph, which normally help eliminate infection. Glyphosate also increased the burden of the malaria-causing parasite Plasmodium falciparum in A. gambiae mosquitoes, altered uninfected mosquito survival, and perturbed the microbial composition of adult mosquito midguts. Our results show that glyphosate’s mechanism of melanin inhibition involves antioxidant synergy and disruption of the reaction oxidation–reduction balance. Overall, these findings suggest that glyphosate’s environmental accumulation could render insects more susceptible to microbial pathogens due to melanin inhibition, immune impairment, and perturbations in microbiota composition, potentially contributing to declines in insect populations.


Parasitology ◽  
2007 ◽  
Vol 134 (14) ◽  
pp. 1931-1939 ◽  
Author(s):  
P. I. FURUTA ◽  
T. W. P. MINEO ◽  
A. O. T. CARRASCO ◽  
G. S. GODOY ◽  
A. A. PINTO ◽  
...  

SUMMARYNeospora caninumcauses economical impact in cattle-raising farms since it is implicated as the major cause of bovine abortions. Although infection by the parasite has been widely described in mammals, the role of birds in its life-cycle is still obscure. Therefore, this work aimed to evaluate the infection byN. caninumin different chicken models. Experimental infections were conducted in 7-day-old chicks, laying hens and embryonated eggs, where samples were analysed for parasite burden, IgG antibodies and lesions promoted. Chickens demonstrated an asymptomatic infection, although with seroconversion and systemic replication of the parasite. In laying hens, no signs of vertical transmission were observed. However, embryonated eggs inoculated by the allantoic cavity route demonstrated susceptibility to infection, with mortality rates around 50% independent of the inoculum dose. Additionally, dogs became infected after ingestion of different amounts of inoculated eggs, producing either oocysts or specific IgG antibodies. The results herein presented demonstrate that chickens may be intermediate hosts ofN. caninumand that embryonated eggs could be a useful model to study the parasite's biology.


PEDIATRICS ◽  
1957 ◽  
Vol 20 (3) ◽  
pp. 431-438
Author(s):  
Benjamin H. Landing ◽  
Harry S. Shirkey

The clinical and pathologic findings in two white male children with repeated infections, including lymphadenitis, aphthous stomatitis, enteritis, pneumonitis, osteomyelities, etc. are described. Tissue removed at laparotomy in one patient, and at necropsy in the other, showed infiltration of organs by lipid histiocytes containing yellow-brown pigment. Although the histochemical properties of the cells show similarities to the lipid histiocytes of Niemann-Pick disease, the condition described is considered to differ from other forms of lipid histiocytosis, as well as from other conditions producing susceptibility to infection. Concentrations of gamma-globulin in the serum of one of the patients were elevated, but whether the globulin is functionally effective is not known. The onset of symptoms in early infancy suggests that the disorder is genetically determined rather than acquired, but no evidence of familial occurrence has been obtained.


2018 ◽  
Vol 84 (13) ◽  
Author(s):  
Kasie Raymann ◽  
Erick V. S. Motta ◽  
Catherine Girard ◽  
Ian M. Riddington ◽  
Jordan A. Dinser ◽  
...  

ABSTRACT Accumulating evidence suggests that pesticides have played a role in the increased rate of honey bee colony loss. One of the most commonly used pesticides in the United States is the neonicotinoid imidacloprid. Although the primary mode of action of imidacloprid is on the insect nervous system, it has also been shown to cause changes in insects' digestive physiology and alter the microbiota of Drosophila melanogaster larvae. The honey bee gut microbiome plays a major role in bee health. Although many studies have shown that imidacloprid affects honey bee behavior, its impact on the microbiome has not been fully elucidated. Here, we investigated the impact of imidacloprid on the gut microbiome composition, survivorship, and susceptibility to pathogens of honey bees. Consistent with other studies, we show that imidacloprid exposure results in an elevated mortality of honey bees in the hive and increases the susceptibility to infection by pathogens. However, we did not find evidence that imidacloprid affects the gut bacterial community of honey bees. Our in vitro experiments demonstrated that honey bee gut bacteria can grow in the presence of imidacloprid, and we found some evidence that imidacloprid can be metabolized in the bee gut environment. However, none of the individual bee gut bacterial species tested could metabolize imidacloprid, suggesting that the observed metabolism of imidacloprid within in vitro bee gut cultures is not caused by the gut bacteria. Overall, our results indicate that imidacloprid causes increased mortality in honey bees, but this mortality does not appear to be linked to the microbiome. IMPORTANCE Growing evidence suggests that the extensive use of pesticides has played a large role in the increased rate of honey bee colony loss. Despite extensive research on the effects of imidacloprid on honey bees, it is still unknown whether it impacts the community structure of the gut microbiome. Here, we investigated the impact of imidacloprid on the gut microbiome composition, survivorship, and susceptibility to pathogens of honey bees. We found that the exposure to imidacloprid resulted in an elevated mortality of honey bees and increased the susceptibility to infection by opportunistic pathogens. However, we did not find evidence that imidacloprid affects the gut microbiome of honey bees. We found some evidence that imidacloprid can be metabolized in the bee gut environment in vitro , but because it is quickly eliminated from the bee, it is unlikely that this metabolism occurs in nature. Thus, imidacloprid causes increased mortality in honey bees, but this does not appear to be linked to the microbiome.


2018 ◽  
Vol 31 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Yan Wang ◽  
Yuanchao Wang

The apoplastic space between the plant cell wall and the plasma membrane constitutes a major battleground for plant-pathogen interactions. To survive in harsh conditions in the plant apoplast, pathogens must cope with various immune responses. During infection, plant pathogens secrete an arsenal of effector proteins into the apoplast milieu, some of which are detected by the plant surveillance system and, thus, activate plant innate immunity. Effectors that evade plant perception act in modulating plant apoplast immunity to favor successful pathogen infection. The concerted actions of apoplastic effectors often determine the outcomes of plant-pathogen interactions. In this review, we summarize current advances on the understanding of apoplastic effectors and highlight the strategies employed by pathogens to counter host apoplastic defense.


2019 ◽  
Author(s):  
Qinghe Li ◽  
Fei Wang ◽  
Qiao Wang ◽  
Maiqing Zheng ◽  
Ranran Liu ◽  
...  

AbstractAs a canonical adaptor for Toll-like receptor (TLR) family, MyD88 has crucial roles in host defence against infection of microbial pathogens and its dysregulation might induce autoimmune diseases. Here we demonstrate that the Cullin 3-based ubiquitin ligase adaptor SPOP recognizes the intermediate domain and degrades chMyD88 through the proteasome pathway. Knockdown or genetic ablation of chSPOP leads to aberrant elevation of the chMyD88 protein. Consequently, ChSPOP negatively regulates the activity of NF-κB pathway and thus the production of IL-1β and IL-8 upon LPS challenge. Furthermore, SPOP deficiency mice are more susceptible to infection of Salmonella typhimurium. Collectively, these findings demonstrate chMyD88 as a bona fide substrate of chSPOP and uncover a mechanism by which chSPOP suppresses the innate immune signaling.Author SummaryMyD88 is a central adaptor mediating the initiate of innate immune response and production of proinflammatory cytokines that restrain pathogens and activate adaptive immunity. Although MyD88 is crucial for the host to prevent pathogenic infection, misregulation of MyD88 abundance might lead to autoimmune diseases. Thus, degradation of MyD88 is a canonical mechanism to terminate cytokines production. Here we characterized a novel E3 ligase SPOP that target MyD88 for degradation. SPOP attenuated IL1β and IL8 production through K48-linked polyubiquitination and degradation of MyD88 and thus impaired immune responses. SPOP deficient mice show more susceptibility to infection by Salmonella typhimurium. These findings demonstrate that SPOP is a negative regulator of MyD88-dependent pathway activation triggered by LPS and Salmonella typhimurium, which helps the host to maintain immune homeostasis.


1962 ◽  
Vol 8 (5) ◽  
pp. 597-602 ◽  
Author(s):  
June M. Stephens

Larval blood of the wax moth, Galleria mellonella (L.), immunized against Pseudomonas aeruginosa does not melanize on exposure to air as does normal blood. Larval blood samples taken 20 to 24 hours after vaccination against either of the pathogens P. aeruginosa or Proteus mirabilis did not melanize; blood of insects vaccinated against the nonpathogenic Shigella dysenteriae strain K 629 or a nonpathogenic strain of Pseudomonas did melanize. Injection of nonspecific agents, such as sodium chloride or egg albumen, did not inhibit melanization. The oxidation–reduction potential of immune blood was markedly lower than that of normal blood. Enzymes from both normal and immune blood were precipitated with cold acetone. The enzyme preparations were nontoxic to normal larvae. Both normal and immune blood enzyme preparations produced melanin from tyrosine, though the immune blood enzyme acted more slowly. Sodium thioglycollate, ascorbic acid, benzoin oxime, and phenylthiourea each inhibited the melanization of normal blood in vitro but did not confer bactericidal activity. These inhibitors did not produce any change in the rate of melanization, bactericidal activity, or immune properties of the blood when injected into larvae.


Author(s):  
S.D. Barnard ◽  
S.D. Warner

1, 2, 9, 10-tetramethoxyaporphine phosphate (MDL-832) was once considered a potential human antitussive. MDL-832 was administered orally in the diets of Sprague-Dawley rats at dose levels of 0, 5, 10, 20, 40, 80 and 160 mg/kg/day for 3 and 6 months and in gelatin capsules to Beagle dogs at 0, 5, 10, 15, 30 and 60 mg/kg/day for 3, 6 and 12 months. Histopathologic examinations of hematoxylin and eosin-stained cerebellar sections revealed intracytoplasmic brown pigment accumulations in large fusiform neurons (presumably the motor type) of the pons. The pigment granules were found to be PAS-positive, non-acid fast, iron-free, Sudan B-positive and fuchsinophilic. Intraneuronal pigment accumulations were seen in rats after 3 months of treatment at 80 mg but not at 40 mg and after 6 months at 20 mg but not at 10 mg. For dogs the effect was observed after 3 months at 60 mg but not at 30 mg and after 12 months at 10 mg but not at 5 mg.


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