Cell-wall deficient bacterial variants in kidney tissue

Dominique, Gerald; Turner, Bruce I.; Schlegel, J.U.

doi:10.1016/s0090-4295(74)80105-6

Cited by 9 publications

(9 citation statements)

References 8 publications

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“…A large number of studies (e.g. Domingue et al ., ; Domingue et al ., ; Domingue & Schlegel, , b ; Domingue & Woody, ; Goubran et al ., ; Mattman, ; Nikkari et al ., ), reviewed previously by Amar et al . (), Kell & Kenny (), Kell et al .…”

Section: Step –1: a Dormant Blood And Tissue Microbiomementioning

confidence: 97%

“…To investigate whether dormant bacteria are present, we thus need culture‐independent methods, of which ultramicroscopic (e.g. Domingue et al ., ; Domingue, , ; Domingue & Woody, ; Ewald, ; Green, Heidger Jr & Domingue, , b ; Mattman, ; Potgieter et al ., ) and molecular sequence‐based methods (Amar et al ., ; Cherkaoui et al ., ; Fernández‐Cruz et al ., ; Gaibani et al ., ; Grif et al ., , b ; C.L. Liu et al ., ; Moriyama et al ., ; NIH HMP Working Group et al ., ; Nikkari et al ., ; Sakka et al ., ; Sato et al ., ; Valencia‐Shelton & Loeffelholz, ; Woyke, Doud & Schulz, ) are by far the most common.…”

Section: Step –1: a Dormant Blood And Tissue Microbiomementioning

confidence: 99%

“…Lauder et al ., ). Indeed, probably all tissues harbour fairly considerable numbers of non‐growing microbes even under normal conditions (Bullman et al ., ; Domingue, Turner & Schlegel, ; Domingue, ; Domingue & Woody, ; Gargano & Hughes, ; Mattman, ; Proal, Albert & Marshall, , ; Proal, Lindseth & Marshall, ).…”

Section: State –2a: Infection Dysbiosis and Atopobiosismentioning

confidence: 99%

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No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

Kell

2018

Biological Reviews

108

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Since the successful conquest of many acute, communicable (infectious) diseases through the use of vaccines and antibiotics, the currently most prevalent diseases are chronic and progressive in nature, and are all accompanied by inflammation. These diseases include neurodegenerative (e.g. Alzheimer's, Parkinson's), vascular (e.g. atherosclerosis, pre‐eclampsia, type 2 diabetes) and autoimmune (e.g. rheumatoid arthritis and multiple sclerosis) diseases that may appear to have little in common. In fact they all share significant features, in particular chronic inflammation and its attendant inflammatory cytokines. Such effects do not happen without underlying and initially ‘external’ causes, and it is of interest to seek these causes. Taking a systems approach, we argue that these causes include (i) stress‐induced iron dysregulation, and (ii) its ability to awaken dormant, non‐replicating microbes with which the host has become infected. Other external causes may be dietary. Such microbes are capable of shedding small, but functionally significant amounts of highly inflammagenic molecules such as lipopolysaccharide and lipoteichoic acid. Sequelae include significant coagulopathies, not least the recently discovered amyloidogenic clotting of blood, leading to cell death and the release of further inflammagens. The extensive evidence discussed here implies, as was found with ulcers, that almost all chronic, infectious diseases do in fact harbour a microbial component. What differs is simply the microbes and the anatomical location from and at which they exert damage. This analysis offers novel avenues for diagnosis and treatment.

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Section: Step –1: a Dormant Blood And Tissue Microbiomementioning

confidence: 97%

Section: Step –1: a Dormant Blood And Tissue Microbiomementioning

confidence: 99%

Section: State –2a: Infection Dysbiosis and Atopobiosismentioning

confidence: 99%

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No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

Kell

2018

Biological Reviews

108

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“…Reducing the ability of the VDR to express elements of innate immune function allows intracellular bacteria to persist in the cytoplasm of nucleated cells and may account for the increased susceptibility to non-bacterial co-infections that are commonly found in patients with chronic illnesses [124, 125]. Theoretically, immune system suppression allows parasitic microbes to persist and proliferate in host phagocytes, successfully compete for nutritional resources, and displace commensal organisms from their niche [126]. Elevated 1,25(OH)2D appears to be evidence of a disabled immune system’s attempt to activate the VDR to combat infection.…”

Section: Effects Of Intracellular Pathogens On the Immune Systemmentioning

confidence: 99%

Inflammation and vitamin D: the infection connection

Mangin¹,

Sinha²,

Fincher³

2014

Inflamm. Res.

231

203

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IntroductionInflammation is believed to be a contributing factor to many chronic diseases. The influence of vitamin D deficiency on inflammation is being explored but studies have not demonstrated a causative effect.MethodsLow serum 25(OH)D is also found in healthy persons exposed to adequate sunlight. Despite increased vitamin D supplementation inflammatory diseases are increasing. The current method of determining vitamin D status may be at fault. The level of 25(OH)D does not always reflect the level of 1,25(OH)2D. Assessment of both metabolites often reveals elevated 1,25(OH)2D, indicating abnormal vitamin D endocrine function.FindingsThis article reviews vitamin D's influence on the immune system, examines the myths regarding vitamin D photosynthesis, discusses ways to accurately assess vitamin D status, describes the risks of supplementation, explains the effect of persistent infection on vitamin D metabolism and presents a novel immunotherapy which provides evidence of an infection connection to inflammation.ConclusionSome authorities now believe that low 25(OH)D is a consequence of chronic inflammation rather than the cause. Research points to a bacterial etiology pathogenesis for an inflammatory disease process which results in high 1,25(OH)2D and low 25(OH)D. Immunotherapy, directed at eradicating persistent intracellular pathogens, corrects dysregulated vitamin D metabolism and resolves inflammatory symptoms.

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“…(18) Especially remarkable findings were that treatment of rats with penicillin induced the formation of stable E. coli L-forms in vivo, and that these L-forms did not cause pyelonephritis but persisted inside the animal causing an asymptomatic infection. (19) The idea that genesis of L-forms might underlie chronic and relapsing bacterial infections received further support from studies showing that streptococcal L-forms are spared from the killing action of the antibody complement system, which acts on cell-wall-containing bacteria only. (20) Furthermore, L-forms are efficiently phagocytized by macrophages, and can survive for long periods within phagocytic cells.…”

Section: Introductionmentioning

confidence: 99%

Bacterial L‐forms require peptidoglycan synthesis for cell division

Casadesús¹

2007

BioEssays

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Cell-wall-less bacterial variants, or L-forms, have been described in many bacterial species under laboratory conditions, in infected eukaryotic cell cultures and inside animals. Of special interest for human health is the formation of L-forms as a consequence of specific antibiotic treatments, and the potential involvement of L-forms in persistent and relapsing infections. An old enigma about L-forms is how they can divide in the absence of cell wall synthesis, since septum formation is an essential requisite for cell division. However, the classical definition of L-forms as cell-wall-less bacterial variants may need a revision to accommodate recent observations by Richard d'Ari and coworkers: genetic and biochemical evidence indicates that E. coli L-forms induced by beta-lactam antibiotics do contain small amounts of peptidoglycan, essential for their growth and probably required for septum formation. If these observations are extrapolated to all known L-forms, the very concept of cell-wall-less bacteria may need revision, and be restricted to mycoplasmas and their relatives.

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Cell-wall deficient bacterial variants in kidney tissue

Cited by 9 publications

References 8 publications

No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

Inflammation and vitamin D: the infection connection

Bacterial L‐forms require peptidoglycan synthesis for cell division

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