micro flora bacteriana
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MICROBIOTA/MICROBIOMA
INTESTINAL
PEDIATRIA
Hospital Alberto Sabogal Sologuren
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• El TGI, va desde
labios hasta ano
•Area más grandecontacto con el
medio externo.
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Definición
• Ecosistema abierto que comprende una
amplia variedad de poblaciones microbianas
metabólicamente activas que coexisten en
una región espacio temporal definida y que
juegan un importante papel en la salud del
huésped.
ALIM. NUTRI. SALUD
Vol. 11, N.º 2, pp. 37-48, 2004
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ALIM. NUTRI. SALUD
Vol. 11, N.º 2, pp. 37-48, 2004
> 95% de
bacterias de la
microbiota
intestinal viven enel colon.
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Desarrollo de la Flora Intestinal
Normal
• Intrautero – el intestino : medio esteril
• Al nacer –
El RN adquiere bacterias del canal del parto y LM – Bifidobacterias y lactobacilos
• Nacidos por CESAREA – Se colonizan del ambiente hospitalario
•Nacidos por VIA VAGINAL – 1° dia de vida: heces : Escherichia coli y Enterococcus
– 5° dia de vida: Bifidobacterium spp
An Pediatr, Monogr. 2006;4(1):12-9
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• Los que reciben LM
– Predominan Bifidobaterias y bacterias
productoras de acido lactico, pocos bacteroides,
clostridios y otras
• Los que reciben FM
– Predominio de bacteroides, clostridium
• el tamaño de estas poblaciones es muyvariable.
An Pediatr, Monogr. 2006;4(1):12-9
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• RNPT, flora intestinal muy pobre
– Numero bajo de especies bacterianas
– Primeros 10 dias: E. coli y Klebsiella spp.,
enterococos como E. faecalis y estafilococos como
Staphylococcus epidermidis, S. aureus y S.
haemolyticus,
–
Bifidobacterias, instalacion mas tardia
An Pediatr, Monogr. 2006;4(1):12-9
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LM y microbiota
• Factores de la LM
• N-acetilglucosamina,
•
Glucosa,• Lactoferrina,
• La galactosa,
• la fructosa• Favorecer el crecimiento de bifidobacterias
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• Introduccion de alimentacionc omplementaria
– Flora intestinal del adulto
– Predominan bacteroides y otras bacterias
gramnegativas
• A los dos años de vida, se establece hasta la
adultez
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ALIM. NUTRI. SALUD
Vol. 11, N.º 2, pp. 37-48, 2004
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Funciones de la Microbiota Intestinal
• Funcion metabolica
– Sintesis de vitaminas: K
– Produccion enzimatica: lactasa
– Trasnformacion de sales biliares
– Digestion y absorcion de nutrientes
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• Funcion trofica
– Nutricion del epitelio intestinal: 50% de energia
aprox es suministrada por la flora intestinal y
estimulan el desarrollo de las vellosidadesintestinales.
• Funcion protectora
–Barrera intestinal
– Barrera mecanica
– Barrera inmunologica
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Interaccion entre el huésped y la
Microbiota intestinal
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(a) During gut homeostasis while maintaining a polarized configuration (with intact
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(a) During gut homeostasis, while maintaining a polarized configuration (with intact
tight junctions), enterocytes are tolerant to TLR stimulation by normal microflora, and
NF-B activation is low. Secretion of -defensin by Paneth cells helps control the amount
of intestinal microflora. PGN, peptidoglycan; CpG, CpG oligo deoxynucleotides; DC,
dendritic cell. (b) Activation of IKK and NF-B in response to trichuris infection results in
TSLP secretion, which 'instructs' dendritic cells to induce a TH2 response with
eosinophils and immunoglobulin E (IgE) –secreting B cells, thus eradicating the parasite.
The -defensins and -defensins secreted by Paneth cells and enterocytes, respectively,
control the microflora. p50 and p65, NF-B subunits. (c) Deficiency in IKK or NEMO
(possibly representing ectodermal dysplasia with immune deficiency) leads to a lack of
TSLP and -defensin production, causing dendritic cells to secrete IL-12 and IL-23, whichinduces a TH1 and IL-17-secreting T helper (TH-17) response and, consequently, a
chronic inflammatory reaction. Tissue damage ensues, due to the accumulation of
neutrophils and other inflammatory cells and the secretion of proapoptotic cytokines
such as TNF. M, macrophage; G-CSF, granulocyte colony-stimulating factor. (d) In
Paneth cells, gain-of-function mutations in the gene encoding Nod2 (mNod2) with
hypersensitivity to muramyl dipeptide (MDP) result in excessive NF-B activation, withsecretion of a hypothetical cytokine that forces DCs to release IL-12 and IL-23. The
outcome is induction of a TH1 and an IL-17-secreting T helper response that promotes
tissue damage and Crohn's colitis. Alternatively, loss-of-function mutations in the gene
encoding Nod2 compromise NF-B activation and the production of a TSLP-like factor,
also resulting in TH1-driven colitis. IFN g-, interferon g-.
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MICROFLORA Y PROBIOTICOS
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(a) During gut homeostasis, while maintaining a polarized configuration (with intact
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( ) g g , g p g (
tight junctions), enterocytes are tolerant to TLR stimulation by normal microflora, and
NF-B activation is low. Secretion of -defensin by Paneth cells helps control the amount
of intestinal microflora. PGN, peptidoglycan; CpG, CpG oligo deoxynucleotides; DC,
dendritic cell. (b) Activation of IKK and NF-B in response to trichuris infection results in
TSLP secretion, which 'instructs' dendritic cells to induce a TH2 response with
eosinophils and immunoglobulin E (IgE) –secreting B cells, thus eradicating the parasite.
The -defensins and -defensins secreted by Paneth cells and enterocytes, respectively,
control the microflora. p50 and p65, NF-B subunits. (c) Deficiency in IKK or NEMO
(possibly representing ectodermal dysplasia with immune deficiency) leads to a lack of
TSLP and -defensin production, causing dendritic cells to secrete IL-12 and IL-23, whichinduces a TH1 and IL-17-secreting T helper (TH-17) response and, consequently, a
chronic inflammatory reaction. Tissue damage ensues, due to the accumulation of
neutrophils and other inflammatory cells and the secretion of proapoptotic cytokines
such as TNF. M, macrophage; G-CSF, granulocyte colony-stimulating factor. (d) In
Paneth cells, gain-of-function mutations in the gene encoding Nod2 (mNod2) with
hypersensitivity to muramyl dipeptide (MDP) result in excessive NF-B activation, withsecretion of a hypothetical cytokine that forces DCs to release IL-12 and IL-23. The
outcome is induction of a TH1 and an IL-17-secreting T helper response that promotes
tissue damage and Crohn's colitis. Alternatively, loss-of-function mutations in the gene
encoding Nod2 compromise NF-B activation and the production of a TSLP-like factor,
also resulting in TH1-driven colitis. IFN g-, interferon g-.
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• In the initial stage of immune response, the innate immune systemrecognizes the presence of pathogens and provides the first line of defense. Dendritic cells which are circulating through the tissue hasthe ability to recognize presence of pathogen associated molecularpatterns or PAMPs. PAPMs are conserved features of pathogenssuch as lipopolysaccharides (LPS) that are components of the cell
membrane of all gram-negative bacteria. Dendritic cells have theability to recognize PAMPs through the expression of family of Tolllike receptors (TLRs). In the case of LPS it is recognize by TLR4receptor, which is expressed in the surface of dendritic cells. LPS istransported by a soluble LPS binding protein (LBP) to the surface of dendritic cells, And it’s deposited in cell surface protein (CD14). The
presence of LPS is detected by TLR4 though its interaction andrecognition of the LPS bound CD14. The signal delivered by TLRinitiates maturation of dendritic cell. Dendritic cell can now migrateto regional lymph nodes and activate required immune response
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• Paso de bacterias viables por el epitelio TGI
• Endotoxinas y bacterias muertas en pequeñascantidades cumple un rol fisiologico.
• estimulo fisiologico – RES (kupffer).• T. bacteriana: predominio de Aerobios gram –
• Escherichia. Proteus. Klebsiella
• Via linfatica –g mesentericos, higado bazo • Generaliza : sepsis, shock, FO multisistemica.
TRANSLOCACION BACTERIANA
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• En modelos animales:
• Shock hemorragico
• Quemaduras
• Trauma
• Isquemia – Obstruccion intestinal
•
Falla aguda hepatica, cirrosis• Pancreatitis severa
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• Sobrecrecimiento intestino delgado.
• Incremento de la permeabilidad de la barrera
mucosa.
• Alteracion de defensas inmuntarias
3 mecanismos:
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• Translocacion B. esta asoacida con desarrollo
de Sepsis post operatoria.
• Cirrosis (sobrecrecimiento bact. Intest.
Delgado), peritonitis espontanea y
complicaciones hepaticas.
ORIGEN DE LOS PROBIÓTICOS
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80
Elie Metchnikoff (1.845 -1.916)
“Ciertas células soncapaces de engullir
cuerpos extraños”.
Probiótico:
“a favor de la vida”
ORIGEN DE LOS PROBIÓTICOS
PROBIÓTICOS
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PROBIÓTICOS
81
” Pr obióticos sonmicrobios vivos en lacomida suplementaria(incluyendo leche
fermentada y productos OTC) que afectanbenéficamente el huesped al mejorar su balance intestinal microbiano.“
Collins MD, Gibson GR, 1999
PROBIÓTICOS:
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PROBIÓTICOS:REQUISITOS (I)
82
• De origen humano
• No ser patógena
• No ser sensible a enzimas proteolíticas
• Ser capaz de vivir en tránsito gástrico
• No conjugarse con sales biliares
• Capacidad de adhesión y colonización
• Adherencia a células epiteliales
PROBIÓTICOS:
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PROBIÓTICOS:REQUISITOS (II)
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• Sobre vivencia en el ecosistema intestinal
• Producción de componentes antimicrobianos
• Permanencia prolongada y estable
• Inmunoestimulación
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INMUNOMODULACIÓN
84
Se basa en tres principios:
• Reconocimiento del antígeno
• Destrucción del mismo
• Regulación del material destruido
Ó Ó
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FUNCIÓN INMUNOLÓGICA
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• Aumenta actividad fagocítica
• Aumenta producción de linfocitos
•
Aumenta actividad de células NK• Reduce producción de citoquinas
• Aumenta producción de Interleuquinas
•
Inhibición de agentes carcinogénicos• Incremento de IgA total y específica
Ó
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FACTORES QUE DISMINUYEN LA POBLACIÓN
DE PROBIÓTICOS
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• Estrés
• Envejecimiento
•Antibioticoterapia
• Quimioterapia y radioterapia
• Anticonceptivos
•
Alcohol• Diarrea intermitente
• Desnutrición
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PRE BIÓTICOS
87
”UN pr ebiótico es un ingrediente selectívamentefermentado que permite cambios específicos, tanto
en la composición y/o actividad en la microflora gastrointestinal, que confiere beneficios en la salud del huesped.”
Gibson GR, Probert HM et al., submitted (2003)
SIMBIÓTICOS
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SIMBIÓTICOS (ALIMENTOS FUNCIONALES)
88
• • PROBIÓTICOS
+
• PREBIÓTICOS
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PROB IÓTICOS (1.965)
PRE B IÓTICOS (1.995)
SIM B IÓTICOS (2 001)
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