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- Comparatively Speaking: Pathogenic vs. Non-pathogenic Bacteria
- Pathogenic and Non-pathogenic Microorganisms and Insects
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Immune priming in insects involves an initial challenge with a non-pathogenic microbe or exposure to a low dose of pathogenic microorganisms, which provides a certain degree of protection against a subsequent pathogenic infection.
The protective effect of insect immune priming has been linked to the activation of humoral or cellular features of the innate immune response during the preliminary challenge, and these effects might last long enough to promote the survival of the infected animal.
The fruit fly Drosophila melanogaster is a superb model to dissect immune priming processes in insects due to the availability of molecular and genetic tools, and the comprehensive understanding of the innate immune response in this organism. Previous investigations have indicated that the D. Here we have extended these studies by examining the result of immune priming against two potent entomopathogenic bacteria, Photorhabdus luminescens and P. We have found that rearing D.
Also, subsequent intrathoracic injection with P. These findings suggest that immune priming in D. Editor: Efthimios M. This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
The work is made available under the Creative Commons CC0 public domain dedication. Data Availability: All relevant data are included in the paper and its Supporting Information files. Competing interests: The authors have declared that no competing interests exist. The previous exposure of an insect host to live or dead microbes can induce immune priming, a process that can promote activation of certain innate immune activities, which can in turn provide a protective effect against a subsequent infection [ 1 ].
Previous evidence suggests the existence of various forms of immune priming effects in different insect species. For instance, Manduca sexta larvae pre-injected with live bacteria of a non-pathogenic strain of E.
Feeding larvae of the cabbage looper Trichoplusia ni on a diet containing or lacking non-pathogenic E. Using a similar experimental setup, honey bee Apis mellifera larvae exposed through feeding to spores of Paenibacillus larvae or to a mix of non-pathogenic bacteria have also exhibited increased upregulation of the antimicrobial peptide gene abaecin [ 4 ].
Also, mRNA levels of cecropin A are notably elevated in the fat body, gut and hemocytes of the silkworm Bombyx mori previously fed on diet supplemented with heat-killed P.
Furthermore, Bombus terrestris bumblebees have increased survival to injection with Pseudomonas fluorescens , Paenibacillus alvei , or P. These findings indicate that immune priming in insects can regulate molecular processes controlling specific immune functions that could then impact the outcome of an infection.
In the D. This proved to be a bacterium-specific effect, which was due to increased activation of the Toll pathway and enhanced phagocytic capacity in the primed flies [ 7 ].
Similarly, D. Although in this case the effect was short-lasting, again it was attributed to changes in humoral and cellular immune activities in the pre-infected insects [ 8 ]. Interestingly, pre-exposure of adult flies through pricking to Drosophila C Virus DCV does not improve their survival to a subsequent infection by pricking with this natural viral pathogen [ 9 ].
These findings indicate that priming efficiency in D. Bacteria from the genus Photorhabdus can act as mutualists and pathogens in different hosts [ 10 ]. The bacteria are vectored in the gut of the infective juvenile stage of the nematodes, which live in the soil and frequently invade susceptible insect larvae. The bacteria are released once the nematodes enter the hemolymph insect blood , where they multiply rapidly and simultaneously produce a diverse range of toxins and metabolites that target vital insect tissues and organs, causing apoptosis of mainly the gut and fat body cells as well as hemocytes that patrol the hemocoel insect body cavity [ 14 ].
The high virulence of P. The related species P. Their pathogenic properties are controlled by molecular regulatory systems that promote bacterial survival and pathogenicity towards insects by preventing hemocyte migration and phagocytosis [ 18 , 19 ]. In the current study, we aimed at examining the priming effect of D.
In particular, our goal was to determine whether pre-exposure of D. In order to identify the effect of bacterial pre-exposure on D. Specifically, emerged larvae were reared in the presence of live E. Analysis of antimicrobial peptide gene expression showed that Diptericin A and Drosomycin transcript levels were not significantly altered in larvae and pupae, but they were significantly increased in young adult flies 1—3 day-old that had been reared in contact with live or heat-killed bacteria compared to non-pre-exposed individuals Fig 1B and 1C ; and S1 and S2 Tables.
A Experimental scheme. Oregon-R wild-type flies P, Parental generation were reared and allowed to oviposit on normal untreated diet. All values were normalized to LB-containing media controls and analyzed using unpaired t-test.
Error bars represent standard error of the mean. D Longevity of D. Fly mortality for each treatment is shown over a day period. We then monitored the life span of D.
During the period between approximately 20 and 40 days, survival curves appeared to separate in a way that could indicate a pattern, but the slight trend proved unsustainable, and was not substantial enough to be attributed to treatment conditions.
Following bacterial pre-exposure, emerged adult flies were aged for 5 to 7 days and then injected with PBS negative control , E. To monitor immune signalling activation in D. We observed higher transcript levels of Diptericin A and Drosomycin at 24 h post injection with E. Similarly, we found that pre-exposure with live or heat-killed bacteria induced transcript levels of Diptericin A at 24 h post injection with P. Oregon-R wild-type flies P, Parental generation were raised and allowed to lay eggs on normal untreated food.
Pre-exposed flies were then injected intrathoracically with phosphate-buffered saline PBS , a non-pathogenic strain of E. After injection, adult flies were incubated in vials containing normal untreated media.
Prior to injection, D. Based on previous evidence [ 1 , 6 , 20 ], we reasoned that wild-type flies pre-exposed to non-pathogenic bacteria during development would potentially survive differently in response to subsequent infection with pathogenic or non-pathogenic bacteria.
Flies were raised in different conditions that included food supplemented with LB medium, and food containing either live or heat-killed E. We monitored the survival of pre-exposed Oregon-R flies following injection with pathogenic P. Flies pre-exposed to either live or heat-killed E.
Also, flies pre-exposed to live or heat-killed E. Flies pre-exposed to either live or heat-killed mix of E. Survival was monitored for 72 hours post injection. Survival experiments were replicated three times and results were analyzed using Log-rank Mantel-Cox test in GraphPad Prism software.
Results from previous studies have indicated that pre-exposure of D. This effect has been attributed mainly to pre-activation of humoral aspects of the insect immune system [ 1 , 20 — 23 ].
Here, we have analyzed the consequences of pre-exposing D. We have found that pre-exposure during development of D. The pre-exposure effect can further trigger the expression of antimicrobial peptide genes upon secondary infection through intrathoracic injection with the entomopathogen Photorhabdus , which is what would be expected from priming [ 20 ].
However, the observed immune activation fails to confer a survival advantage to the bacterially pre-exposed flies when subsequently infected with either species of Photorhabdus. Our current results denote that maintaining D. However, injection of live or dead E. These results suggest that induction of certain immune signaling pathways in D. Therefore, given that the Imd pathway is mainly induced in the fat body and gut of D. Our results also reveal that raising D. These findings suggest that although Imd and Toll pathways are not substantially induced in larvae and pupae, but only in young adult flies, being in contact with non-pathogenic bacteria, the activity of both pathways can be enhanced substantially in flies experiencing a secondary infection with pathogenic or non-pathogenic bacteria, such as E.
The late upregulation of Imd signaling in response to Photorhabdus injection might be due to the activation of the immune receptor Persephone which is able to sense a broad range of microbes through virulence factor activities rather than molecular patterns [ 27 ]. Similar to our results, larvae of the mosquito Aedes aegypti fed on E. Of note, reduced antimicrobial peptide gene expression in insects pre-exposed to non-pathogenic bacteria compared to untreated controls has not been shown so far.
Overall, previous and current findings indicate that priming of the insect antibacterial immune response can vary greatly according to the insect species, the specific tissues examined, the type of microbe used as priming agent, and the type of pathogen used for secondary challenge.
We have found that longevity is not affected when rearing D. These findings signify that induction of the antibacterial peptide response in primed D. In line with the current results, Imd and Toll signaling can be activated in response to P.
Previous studies have further reported that pre-injection or oral infection of certain insect species with non-pathogenic bacteria can either confer a protective effect or provide no substantial survival advantage to secondary pathogenic infection. For instance, pricking of D. Similarly, injection of pea aphids Acyrthosiphon pisum to a heat-killed mix of E. In contrast, oral exposure of red flour beetle Tribolium castaneum larvae to liquid media previously used for growing Bacillus thuringiensis spores confers a bacterial strain-specific priming effect by promoting survival to oral infection with this insect pathogen [ 31 ].
A bacterial species-specific survival protective effect has also been documented for the tiger moth Parasemia plantaginis when larvae are orally exposed to a non-lethal dose of the pathogenic bacteria S. In addition, B. In conclusion, in the present study we have shown that the constant presence of non-pathogenic bacteria during the development of D. These findings, in combination with previous reports [ 9 , 30 ], support the notion that priming of D. Identifying the exact basis for variation in immune priming capacity of D.
Wild-type Oregon-R flies were raised on standard cornmeal-soy based food Cat. Supernatants were discarded and pellets were washed with 10 ml of sterile 1X phosphate buffered saline PBS Sigma. For treatments with live bacteria, E. For treatments with heat-killed bacteria, E. Three replicates of five male and female adult flies were initially reared on normal fly food, as described in Fig 1A , P arental panel.
After two days of egg laying, parent adult flies were removed, leaving only progeny F1 in the vials. Five male and five female newly emerged flies Fig 1 , F1 from each treatment condition were placed in vials containing untreated food. Fly mortality was assessed every 24 hours until mortality for each treatment reached one hundred percent.
Longevity curves were generated from three independent trials.
Comparatively Speaking: Pathogenic vs. Non-pathogenic Bacteria
The terms pathogenic and non-pathogenic are often are applied to various microbes. By definition, a pathogen is a specific cause of a disease, while a non-pathogen is considered harmless. In reality, the distinction is not always clear. In , the German physician Robert Koch formalized the criteria to classify bacteria as pathogenic. See Koch's Postulates. While these definitions made sense at the time, advances in microbial sampling and identification have shown that they are unable to account for microbes that cause disease in some individuals but are also present in normal individuals without causing disease.
Antibiotic resistance genes in food and gut non pathogenic bacteria. Bad genes in good bugs View all 8 Articles. Some ecosystems are inhabited by an extraordinarily dense population of microbes, such as fermented foods. Their microbial load can reach higher than one billion microorganisms per gram, although the bacterial diversity is normally low due to the prevalence of a few strains which rapidly adapt to a quickly changing environment. Even higher microbial numbers can be present along the human intestinal tract; however in this case the bacterial diversity is much higher comprising hundreds of different species.
Pathogenic and Non-pathogenic Microorganisms and Insects
J Food Prot 1 April ; 82 4 : — This study investigated the effects of enzyme application on biofilms of bacterial isolates from a cafeteria kitchen and foodborne pathogens and the susceptibility of Salmonella biofilms to proteinase K combined with chlorine treatment. The results showed that certain enzymes inhibited biofilm formation by the kitchen-originated bacteria; however, the enzymatic effect was diminished on the mature biofilms.
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Not a MyNAP member yet? Register for a free account to start saving and receiving special member only perks. The transmission of infectious diseases via contaminated water continues to be a risk to public health in the United States and throughout the rest of the. Source and finished drinking waters are vulnerable to microbial pathogen contamination from a variety of sources of human and animal fecal wastes and from the introduction and proliferation of nonfecal pathogenic microbes. Throughout most of the modem history of drinking water supply, concerns about pathogenic microbes have focused on enteric bacteria of human fecal origin.
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The olefinic gas ethylene ethene is the most unusual and perhaps powerful of the growth-regulating chemicals produced by microorganisms and by healthy and diseased plants. The earliest observations of the physiological effects of the gas by F ahnstock and G irardin , A beles were in relation to damage to coleus plants and lime Tilia vulgaris trees by fuel coal gas contaminated by ethylene. The effects of ethylene on lime trees closely simulated the disease syndrome associated with vascular wilt pathogens such as the Dutch elm disease fungus Ceratocystis ulmi on elm, but it was many years later that its biosynthesis by microorganisms including fungal and bacterial vascular pathogens was established P egg b. Unable to display preview. Download preview PDF.
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